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OF  CALIFORNIA 

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GIFT  OF 
Robert  Huebert 


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http://www.archive.org/details/diseasesofthyroiOOhertiala 


DISEASES  OF  THE  THYROID  GLAND 


DISEASES 

OF  THE 

THYROID    GLAND 


BY 

ARTHUK  E.  HEKTZLER,  M.D.,  F.A.C.S. 

PKOKESSOK  OF  ST'KGEKY  IN  THE  UXmiRSITY  OF  KANSAS   SCHOOL  OF   MEDICINE; 
SURGEON    TO   THE    HALSTEAD    HOSPITAL,    HALSTEAP,    KAXSAS;    SURGEON 
TO   ST.   LUKES   HOSPITAL   AND   ST.   MARYS   HOSPITAL,   KANSAS 
CITY,    MO.,    AND    TO    PROVIDENT    HOSPITAL, 
KANSAS  CITY,  KANSAS. 


WITH  A  CHAPTER  ON 

HOSPITAL  :maxagement  of  goiter  patients 

BY  VICTOR  E.  ,CHESKY,  A.B.,  M.D. 
ASSOCIATE   SURGEON-  TO   HALSTEAD  HOSPITAL 


ONE  HUNDRED  SIX  ORIGINAL  ILLUSTRATIONS 


ST.  LOUIS 
C.  V.  MOSBY  COMPANY 

1922 


CoPYiuciiT,  19122,  BY  The  C.  V.  Mosby  Company 

(All    lights    rcscrz'cd) 


(Piiiited   in   U.    S.   A.) 


Press  of 

The  C.  V.  Mosiy  Company 

St.  Louis 


BismedicaJ 
Library 

PREFACE 

It  is  a  new  departure  for  the  small  country  hospital  to  pre- 
sent to  the  profession  the  result  of  studies  of  any  particular 
disease.  The  disadvantages  detached  workers  labor  under  are 
many,  but  the  advantages  also  are  worth  noting.  The  isolation 
makes  the  investigators  more  free  to  follow  their  own  ideas  un- 
influenced by  the  opinion  of  associates.  The  small  country'  hos- 
pital drawing  its  j)atrons  from  the  immediate  conununity  is 
better  able  to  study  the  end  results.  It  is  only  by  frequent  ex- 
amination of  the  patient  that  one  can  obtain  an  accurate  idea 
of  the  sul)sequent  course  in  disease  of  the  thyroid  gland. 

The  material  obtained  at  operations  has  been  carefully  stud- 
ied and  compared  with  the  clinical  history.  Each  time  informa- 
tion has  been  obtained  as  to  the  subsequent  course  of  the  dis- 
ease the  specimen  and  slide  have  been  re-examined  and  com- 
pared with  the  sum  total  of  information  available  to  date.  This 
study  has  brought  convincing  evidence  that  the  activity  of  the 
interstitial  cells  is  associated  with  a  definite  clinical  type  of 
thyroid  intoxication.  It  is  the  desire  to  bring  this  evidence  be- 
fore the  profession  that  has  prompted  the  publication  of  this 
monograph  at  this  time. 

The  presentation  of  statistics  has  been  designedly  avoided. 
The  study  of  our  cases  has  brought  evidence  that  statistics  as 
now  published  are  of  little  value.  They  present  the  disease  in  an 
entirely  too  optimistic  light  and  the  permanent  value  of  any 
treatment  is  entirely  overestimated.  Statistics  can  be  of  value 
only  when  the  entire  subsequent  life  span  of  the  individual  is 
taken  into  account.  This  obviously  is  not  within  the  range  of 
any  individual  observerT)ut  falls  within  the  province  of  an  in- 
stitution and  particularly  within  the  province  of  the  small  coni- 
nmnity  hospital  v.iiich  serves  a  relatively  stable  population.  It 
is  to  be  hoped  that  tlie  pursuit  of  this  policy  may  in  time  pre- 
sent a  true  picture  of  the  life  history  of  the  disease.    It  is  to  be 

7 


•^06084 


0  PltKFACE 

li()l)od  otlioi"  iiislitutioiis  may  ('iii>a,<>('  in  the  coliectioii  of  similar 
data. 

I  am  i'ortuiiato  to  bo  ahle  to  present  a  series  of  drawings 
made  by  Tom  Jones  illustrating-  tlie  topographic  anatomy  and 
the  ope]-ative  technie  of  the  operations  on  the  thyroid  gland  as 
done  in  this  hospital.  The  preliminary  sketches  were  made  be- 
side the  o])erating  table  and  present  the  various  steps  with  more 
than  the  avei-age  degree  of  accuracy. 

A.  E.  H. 

iliilstcad,  Kansas. 


CONTENTS 


CHAPTER  I 

Page 

Etiology   and   Pathogknk5;is    of    Goiter 17 

Age,  17;  Sex,  IS;  Herodity,  20;  Endemiology,  21;  Infection,  22;  Previous 
and     Associated     Diseases,     23;     Xeurogeiiic     Theories,     23;     Thyi'Ogenic 
Theory,  25, 

CHAPTER  II 

J\ORMAi,  AND  Pathologic  Anatomy  of  the  Thyroid  Gland 28 

Normal  Morpliology,  2S;  Pathological  Anatomy,  41;  Colloid  Goiter,  43; 
Adenomatous  Goiter,  5:-);  Interstitial  Proliferative  Goiters  (Forme  Fruste), 
70;  Pathology  of  Other  Organs  Associated  with  Goiter,  79;  General 
Summary,  84. 

CHAPTER  III 

Symptomatology  of  Diseases  of  the  Thyroid  Gland     ,  85 

Goiter,  85 ;  Degree  of  Enlargement,  85  ;  Consistency,  87 ;  Sensitiveness,  88 ; 
Mobility,  88 ;  Eye  Symptoms,  88 ;  Exophthalmia.,  89 ;  Imperfect  Movement 
of  the  Upper  Lid,  90 ;  Graef e  's  Sign,  91 ;  Lessening  of  Involuntary  Wink- 
ing, 91;  Disturbance  of  Convergence,  92;  Uncommon  Eye  Signs,  93;  Pupil 
sign,  93;  Field  of  Vi.sion,  93;  Tear  Secretion,  93;  Nystagmus,  93;  Involve- 
ment of  the  Muscular  System,  94;  Tremor,  94;  Muscular  Fatigue,  94;  The 
Heart  in  Thyroid  Disease,  95;  Tachycardia,  96;  Blood  Pressure,  97;  Heart 
Sounds,  99;  Goiter  Heart,  99;  Thyrotoxic  Heart,  100;  Mechanical  Goiter 
Heart,  100;  Digestive  Disturbance,  102;  The  Appetite,  102;  Diarrhea, 
102;  Vomiting,  102;  Constipation,  103;  Icterus,  103;  Intestinal  Hemor- 
rhages, 104;  Clianges  in  the  Skin,  104;  Blood  Changes,  105;  Anemia, 
105;  Leucoeytosis,  lOG;  Changes  in  Coagulation  Time,  108;  The  Goetsch 
Test,  108;    The  Adrenalin   Test,   109;   Basal  Metabolism,   110. 

CHAPTER  IV 
Diagnosis  of  Thyroid  Disease 112 

Colloid  Goiter,  ]12;  Adolescent  Goiter,  112;  Simple  Colloid  Goiters,  113; 
Secondary  Toxicity,  114;  Malignant  Degeneration,  114;  Affections  of 
Other  Organs,  115;  Toxic  Goiter,  116;  Secondary  Toxic  Goiter,  117; 
Atypical    Forms,    llil;    Hyperacute    Forms,    119;    Forme    Fruste,    120. 

CHAPTER  V 

Prognosis    in   Disease  of   the   Thyroid 125 

Malignancy,    131;    Mortality    ofter    Operation,    131. 

9 


10  CONTENTS 

CHAPTER  \1 

Page 

Goiters  in  Unusual  Places 133 

Abnormal  Expansion  of  the  Normally  Sitiiatod  Thyroid  Gland,  133;  Sub- 
sternal and  Intrathoracic   Goiter,  138;   Aberrant  Goiters,   149. 

CHAPTER  YII 
Hospital  Management  of  Goiter  Patients.  By  Dr.  Victor  E.  Chesky  .  156 
Preoperative  Treatment,  1.36;  Nontoxic  Goiter,  156;  Toxic  Goiters,  156; 
Postoperative  Treatment,  161;  Postoperative  Complications,  166;  Collapse 
of  the  Trachea,  16(3;  Hemorrhage,  167;  Hoarseness,  Loss  of  Voice,  Paral- 
ysis of  Vocal  Cords,  168;  Shock,  169;  Acidosis,  169;  Infection,  170; 
Disfiguring  Scars,  171;  Bronchitis  and  Pneumonia,  172;  Tetany,  172; 
Myxedema,  173;   Instructions  at  Dismissal,  174. 

CHAPTER  VIII 

'J'reatment  of  Diseases  of  the  Thyroid  Gland 175 

Adolescent  Goiter,  176;  Colloid  Goiter  in  the  Adult,  179;  Primary  Toxic 
Goiter,  181;  Secondary  Toxic  Goiter,  181;  Forme  Fruste  (Interstitial), 
183. 

CHAPTER  IX 

Topographic  Anatomy  of  the  Thyroid  Gland 185 

The  Overlying  Soft  Parts,  185;  The  Skin  Covering,  185;  The  Platysma 
Myoides,  186;  The  Superficial  Veins,  186;  The  Muscles  of  the  Neck,  188; 
The  False  Capsule,  190;  The  Nerve  Supply  of  the  Skin  and  Muscles,  190; 
The  Nerve  Supply  of  the  Thyroid  Gland,  193 ;  The  Sympathetic  Nerves, 
193 ;  The  Superior  Laryngeal  Nerves,  193 ;  The  Recurrent  Laryngeal 
Nerves,  193;  Topography  of  the  Gland,  194;  The  Blood  Supply  of  the 
Thyroid  Gland,  194 ;  The  Arteries  of  the  Thyroid  Gland,  196 ;  The  Superior 
Thyroid  Arteries,  196;  The  Artery  to  the  Suspensory  Ligament,  196;  The 
Inferior  Thyroid  Arteries,  198 ;  The  Thyroidea  Ima  Artery,  198 ;  Disturb- 
ance of  the  Site  of  the  Vessels  by  Thyroid  Hypertrophy,  200. 

CHAPTER  X 

Technic  of  Operations  on  the  Thyroid    Gland 205 

The  Anesthetic,  206;  The  Skin  Incision,  214;  Incision  of  the  Platysma, 
214;  Incision  of  the  Deep  Muscles  of  the  Neck,  215;  Isolation  of  the  Su- 
perior Pole,  217;  Separation  of  the  Lateral  Border  and  Ligation  of  the 
Lateral  Vessels,  220;  Dislocation  of  the  Lower  Pole,  221;  Dislocation  of 
the  Lobe,  224;  Excision  of  the  Lobe,  224;  Disposal  of  the  Pole  Stumps, 
229;  Management  of  the  Second  Lobe,  229;  Closure  of  the  Wound,  230; 
Sutures  Used,  233;   Drainage,   236;   Pole  Ligation,   236. 


ILLUSTRATIONS 


I'lG.  Page 

1.  Slide  of  a  normal  thyroid  gland  showing  the  thin  fibrous  tissue  capsule      .       29 

2.  High  power  of  the  preceding  slide  showing  the  large  nucleated  cells  lying 

between  the  fiber  bundles  which  compose  the  capsule 29 

3.  tSiide  of  a  normal  thyroid  gland  from  which  the   superficial  layer  of   the 

fibrous  ciipsule  has  been  teased  off  to  show  its  endothelial-like  char- 
acter      30 

4.  Slide   of   a   nornial   thyroid   gland   showing   the   septa   which  separate   the 

gland    into   secondary    lobules 30 

5.  Slide    showing   the    sustentacular    tissue    between   the   acini   teased   apart. 

The  thin  planes  of  tissue  with  small  spindleform  cells  are  shown     .        31 

6.  Cross  section  of  a  superior  thyroid  artery  just  below  the   surface  of  the 

gland,     showing    the    thick     walls 31 

7.  Injected  gland  showing  the  network  of  capillaries  in  the  interacinal  spaces       32 

8.  Slide  showin<;  a  sujx'rficial  vein  of  a  normal  thyroid  gland 33 

P.  Slide  from  a  normal  thyroid  gland  showing  the  variation  in  size  and  form 

of    the    acini 35 

10.  High  power  of  the  preceding  showing  the  form  and  relation  of  the  acinal 

cells 36 

11.  Slide  from  an  old  colloid  goiter  pliowing  the  thin  interacinal  septac  and  the 

low  endothelial-like  acinal  cells  37 

12.  Slide  of  a  thyroid  gland  taken  from  a  boy  aged  four,  showing  interstitial 

cells  and  their  relation   to  the  acinal  cells 38 

13.  Slide  from  a  slightly  toxic  goiter  (forme  fruste)   showing  the  acinal  cells 

inactive   Avhile   the  interstitial  cells   arc   active 39 

14.  Slide  obtained  from  a  boy  aged  four  years  made  from  tissue  removed  during 

an  operation  for  intratracheal  growth 40 

15.  Section  of  a  small  recent  colloid  goiter  showing  the  uniform  granular  sur- 

face      44 

16.  A  colloid  goiter  of  medium  size  showing  the  translucent  masses  of  colloid 

and  the  mildly  bosselated  surface  showing  the  position   of  the  chief 
colloid  masses 44 

17.  Section  of  a  large  coloid  goiter  of  long  duration  showing  degeneration  with 

secondary      hemorrhages 45 

18.  Section  of  a  colloid  goiter  of  45  years'  duration  which  has  undergone  ex- 

tensive fibrous  degeneration 46 

19.  Section  of  a  large  colloid  goiter  showing  uniform  enlargement  of  the  thy- 

roid lobe  with  the  retention  of   the  original  lobulations 46 

20.  Section   of  an  old  colloid  goiter  showing  the  unequal  development  of  the 

lolniles 47 

21.  Slide  of  an  early  colloid  goiter  showing  the  uniform  increase  of  the  colloid 

without  changes  of  the  acinal  epithelium  or  retraction  or  vacuolization 

of  the  colloid 48 

11 


12  ILLUSTRATIONS 

Fig.  Page 

22.  Slide  showing  the  flat,  inactive  cells  of  a  quiescent  colioid  goiter     .  .       49 

23.  Slide  from  a  clinically  inactive  goiter 50 

21.  Slide  of  a  supposedly  inactive  goiter 51 

25.  Section  of  an  old  colloid  goiter     ....  52 

26.  Sections  of  cysts  of  the  thyroid  showing  an  old  clot  indicating  an  ancient 

process,    and    a    recent    hemorrhage 53 

27.  Section  of  a  thyroid  showing  many  degeneration  cysts  which  collapsed  dur- 

ing the   operation,  and  the  more  recent   lobe   showing  beginning  col- 
loid  degeneration 54 

28.  Slide   of  a  goiter   which  has   undergone   fibrous   degeneration     ....       55 

29.  Section   of  a   large  goiter   of  long   duration   showing   extensive   calcareous' 

degeneration. 56 

30.  Slide  of  an  old  goiter  showing  activity  of  the  interstitial  cells  with  fibrosis 

and     secondary     hyaline     degeneration 57 

31.  Slide  of  an  "innocent"  goiter  of  forty-five  years'  duration     ....  57 

32.  Slide  of  an  adenomatous  goiter  which  caused  extensive  bone  metastasis     .  58 

33.  I'hotograpli    of   a    fetal   adenoma   showing   its    smooth   ovoid   contour   and 

the    uniform    fine   granular   character    of   the    cut    surface     ....       60 

34.  Section  of  an  old  fetal  adenoma  which  has  undergone  complete  degenera- 

tion with  secondary  hemorrhage  and  cyst  formation 60 

35.  Slide  of  a  fetal  adenoma  sho-wing  the  small  acini  with  little  colloid     .      .        61 

36.  Slide  of  a  toxic  fetal  adenoma   showing  the  presence  of  colloid  in  many 

of    the    acini 62 

37.  Section   of   a    large   colloid   goiter   enclosing    within  itself   a   small    fetal 

adenoma 62 

38.  Slide  of  the  preceding  showing  the  structure   of   the   fetal    adenomatous 

nodule,  and  that  of  the  colloid  part 63 

39.  Section  of  a  recent  acutely  toxic  adenomatous  goiter  showing  fine  granular 

appearance 63 

40.  Section  of  an  adenomatous  goiter  of  a  year 's  duration     ......  64 

41.  Slide  showing  a  typical  picture  of  toxic  goiter  without  eye  signs     .      .  65 

42.  Slide  of  a  toxic  nonexophthalmic  goiter  showing  the  development  of  sec- 

ondary    acini 66 

43.  Slide   from   a   goiter   of   extreme   toxicity 67 

44.  Slide  from  a  typical  exophthalmic  goiter 67 

45.  Slide  from  a  goiter  in  which  the  eye  signs  developed  after  the  api)earance 

of     the     toxicity 68 

46.  High  power  photograph  of  the-acinal  cells  of  an  exophthalmic  goiter     .      .        69 

47.  Slide   showing   extensive   secondary   degeneration   in   a  primary   toxic   ade- 

nomatous goiter 69 

48.  Slide  showing  the  exfoliation  of  the  acinal  cells  in  an  acutely  fatal  case 

of  toxic  goiter 70 

49.  Slide  showing  degeneration  of  the  acinal  cells  and  the  colloid  in  a  second- 

ary   toxic    goiter 72 

50.  Slide  showing  separation  of  the  acinal  cells  from  the  connective  tissue  in 

a  secondary  toxic  goiter 73 

51.  Slide  from  a  secondary  toxic  goiter  showing  the  acinal  cells  in  the  midst 

of     the     colloid     substance 73 


ILLUSTKATiOXS  13 

Fig.  Page 

52.  Slide    from    a    secondary   toxic    goitor    showing-    the    rejuvenescence   of    the 

acinal  cells 74 

53.  Slide  from  a  secondary  toxic  goiter  sliowing  papillary  formation     ...  75 

54.  Slide  from  a  forme  fruste  goiter  showing  activity  in  the  interstitial  cells 

with  little  change  in  the  acinal  cells  or  in  the  colloid 76 

55.  Slide  from  a  forme  fruste  showing  marked  increase  in  the  interstitial  cells 

with    degeneration    of    the    colloid    substance 77 

56.  Slide  from  a  forme  fruste  showing  extensive  proliferation  of  the  interstitial 

cells   with    little   evidence    of    colloid    sulistance 77 

57.  Slide   from  a   forme   fruste   showing   extensive   proliferation   of   the   inter- 

stitial  cells,   and    round-cell   infiltration 78 

58.  Section  of  two  cases  of  forme  fruste  showing  the  fine  granular  surface     .  78 

59.  Showing  the  trachea  as  being  compressed  between  the  lobes  of  the  goiter 

producing  the    so-called   sword  sheath    trachea 134 

60.  Diagram  showing  the  manner  in  which  a  lobe  may  grow  between  the  trachea 

and  esophagus,  comj^ressing  both  these  tubes 134 

61.  Photograph  of  a  specimen  in  which  the  rounded  lobe  on  the  right  lay  be- 

tween the  trachea  and  the  esophagTis  producing  dyspnea  and  dysphasia  135 

62.  X-ray   picture   showing  the   trachea   pushed   far   to  the   left   by   a   medial 

lying    substernal    goiter 136 

63.  X-ray  of  a  goiter  in  which  the  calcareous  plaque  caused  misjudgmeut  as 

to  the  location  of  the  trachea 137 

64.  Diagram  showing  the  difference  between  a  substernal  and  an  intrathoracic 

goiter 139 

65.  Photograph  of  a  patient  who  had  a  typical  exophthalmic  goiter  with  no 

apparent     thyroid     enlargement         141 

66.  Intrathoracic  goiter  in  a  patient  with  dysphagia  and  cough      ....  146 

07.  Diagram   showing   the   possibilities   in   aberrant   goiters 149 

i}S.  An  aberrant  goiter  near   the   angle   of   the   jaw 152 

69.  Intratracheal   goiter .      .  154 

70.  ^Musculature   of   the   neck 187 

71.  The  relation  of  the  anterior  and   the  external  jugular   veins     ....  189 

72.  Musculature   of  the   neck 191 

73.  The   nerve   supply   of   the   neck 192 

74.  The  general  topographic  relations  of  the  thyroid  gland 195 

75.  The  arterial  supply  of  the  thyroid  gland 197 

76.  The  arteries  of  the  thyroid  gland  and  the  recurrent  laryngeal  nerve     .      .  199 

77.  Aberrant    locations    of    the    thyroid    arteries 201 

78.  Veins   of   the   thyroid   gland 203 

79.  Typical  sites  for  ligation  of  the  thyroid  vessels 204 

80.  The    preliminary    needle    prick 210 

81.  The  line  of  primary  infiltration 211 

82.  Intramuscular   infiltration     .      .  ' 212 

83.  Periglandular    infiltration 213 

84.  The   preliminary   incision 215 

85.  Exposure  of  the  anterior  jugular  veins 216 

86.  Ligation  of  the  anterior  jugular  A'eins 217 

87.  Incision  of  the  short  muscles  covering  the  gland 218 

88.  Ligation  of  the  vessels  to  the  isthmus 219 


14  ILLUSTRATIONS 

Fig,  Page 

89.  Separation  of  the  sui^erior  pole  from  the  tracliea 220 

90.  Ligation  of  the  upper  pole 221 

91.  Ligation    of  the  lateral    veins '.      .  222 

92.  Ligation  of  the  inferior  thyroid   artery  and   veins 223 

93.  Topography  of  the  lateral  veins 223 

94.  Wrong  method  of  managing  the   lateral   veins 225 

95.  Diagram  showing  the  appearance  after  the  resection  of  both  lobes      .      .  22(5 

96.  Resection    of    the    gland 226 

97.  Completed    resection    of    the    right    lobe 227 

98.  The  folding   downwards   of   the  npper   pole 228 

99.  The  folding  of  the  poles  completed;   resection  of  the  remaining  lobe     .  230 

100.  Wedge  resection  of  the  opposite  lobe 231 

101.  The  resection   completed 232 

102.  The  closure   of  the  capsule 232 

103.  The  restoration  of  the  sternohyoid  muscles 233 

104.  The  coaptation  of   the   platysma   muscle 234 

105.  The  coaptation  of  the  subcutaneous  fat 234 

106.  The  closure  of  the  skin 235 


DISEASES  OF  THE  THYROID  GLAND 


DISEASES  OF  THE  THYROID  GLAND 


CHAPTER  I 

ETIOLOGY  AND  PATHOGENESIS  OF  GOITER 

As  is  true  of  many  cliroiiic  diseases,  we  <lo  not  know  the 
cause  of  goiter  and  we  can  but  detail  some  of  tlie  conditions  and 
circumstances  under  wliich  it  arises.  The  knowledge  we  pos- 
sess relative  to  the  causation  is  a  matter  of  general  interest  only. 
It  is  quite  useless  in  the  practical  consideration  of  a  concrete 
case.  There  is  an  obvious  diiference  between  the  onset  and  most 
likely  the  causes  of  the  various  kinds  of  goiters.  The  simple 
colloid  and  the  frankly  exophthalmic  type  bear  little  resem- 
I)lance  to  each  other  at  the  outset.  There  are  so  many  transi- 
tional types,  however,  that  it  seems  best  to  consider  all  types 
together.  By  this  means  it  is  possible  to  emphasize  the  very 
obvious  fact  that  there  are  no  "innocent"  goiters.  This  may 
not  ajjply  to  all  regions  and  countries  but  it  surely  does  to 
Kansas. 

Age 

Congenital  goiters  have  been  reported,  but  they  are  rare 
and  are  often  associated  with  other  developmental  anomalies. 
1  have  seen  one  in  a  baby  of  three  days,  otherwise  normal.  Oc- 
casionally patients  of  a  very  early  age  are  met.  I  have  seen  a 
simple  goiter  in  a  girl  of  two  and  a  half  years,  and  typical  exoph- 
thalmic goiter  in  a  girl  of  eight  years,  and  many  about  the  age 
of  puberty. 

The  adolescent  colloid  goiter  occurs  usually  between  the 
tenth  and  twentieth  year.  It  is  only  in  regions  where  the  en- 
ilemic  goiters  are  rare  that  the  age  onset  can  be  accurately  ob- 
served. The  endemic  goiters  usually  appear  in  early  life 
because  the  patients  are  born  in  the  goitrous  regions.  The  ad- 
olescent type  often  disapjiears  after  full  maturity,  possibly  to 
recur  during  the  child-bearing  years. 

17 


18  DISEASES   OF   THE   THYROID   GLAl^D 

The  true  degenerative  toxic  goiter  usually  appears  in  mid- 
dle or  later  life.  The  eoninion  age  of  the  primary  toxic  type,  ac- 
cording to  Sattler,  is  between  twenty  and  forty  years  with  more 
than  half  coming  between  twenty  and  thirty  (55.7  per  cent). 
The  most  violently  toxic  forms  predominate  in  the  fourth  dec- 
ade. The  secondary  toxic  type  is  most  common  after  thirty. 
The  true  degenerative  type  is  seen  most  often  after  the  fiftieth 
year.  The  sudden  appearance  of  the  secondary  type  after  the 
sixtieth  year  is  distressingly  common  though  numerically  the 
more  cases  occur  between  forty  and  sixty.  The  forme  fruste  is 
commonly  seen  in  early  life  though  it  ma}^  appear  at  any  age. 
Stern  found  45.1  per  cent  between  ten  and  twenty,  and  29.4  per 
cent  between  forty  and  sixty,  and  but  9.8  per  cent  between 
twenty  and  forty.  Usually  the  time  of  onset  is  hard  to  deter- 
mine, for  they  give  a  history  of  a  long  enduring  nervousness  and 
are  unconscious  of  the  existence  of  a  goiter. 

Goiters  producing  pressure  symiDtoms  and  the  malignant  de- 
generations occur  in  the  latter  part  of  life.  However,  I  have 
seen  bone  metastases  in  a  patient  twenty-three  years  of  age. 

Sex 

AVomen  are  much  more  prone  to  be  affected  by  goiter.  The 
proportion  is  variously  given  as  from  1:6  to  1:10.  The  dispro- 
portion is  less  in  the  more  severe  forms  than  in  the  milder  types. 
The  reason  goiters  are  more  common  in  women  than  in  men  was 
formerly  based  on  the  knowledge  that  there  was  a  close  associa- 
tion between  the  genital  function  and  the  thyroid  gland.  This 
association  is  indicated  in  the  slight  enlargement  often  seen 
during  menstruation,  and  still  more  during  pregnancy.  The 
adolescent  goiters  of  girls  are  so  closely  associated  with  the  ad- 
vent of  the  menses  that  a  relationship  has  been  assumed.  The 
observation  has  been  made  that  the  reason  women  are  more 
often  affected  by  goiter  is  that  they  are  females,  that  is  to  say, 
that  in  the  complex  adjustment  of  their  horizon  to  the  horizon 
of  the  world  in  general  certain  irritative  products  are  produced 
which  stimulate  the  thyroid  gland  to  development.  Such  specu- 
lations do  not  account  for  the  well-known  geographic  distribu- 
tion of  goiter.  At  any  rate  in  this  time  of  intensive  ductless 
gland  study,  it  is  well  to  remember  that  the  ovary  is  not  the 


ETIOLOGY    AXD    PATHOGENESIS  19 

sole  possible  factor  in  the  preponderance  of  goiter  in  women. 
The  whole  physiologic  metabolism  is  upset  periodically  at  the 
menstrual  periods  and  during  pregnancy  and  its  significance  we 
cannot  now  estimate. 

Clenital  disturbances  of  a  more  indistinct  physiologic  na- 
ture are  sometimes  operative,  possibly  more  often  than  we 
know.  This  disturbance  may  be  due  to  a  conscious  or  uncon- 
scious lack  of  proper  functional  exercise  or  to  overindulgence 
or  sometimes  to  an  improper  exercise  of  that  function.  AVe  need 
not  be  dependent  upon  the  patient's  viewpoint  alone.  When 
we  suspect  that  one  of  these  factors  is  influencing  the  condition, 
improvement  may  follow  its  correction.  Xot  infrequently  a 
toxic  goiter  improves  by  marriage  and  childbirth.  Conversely 
toxic  goiter  may  arise  during  pregnancy  or  be  made  worse  by 
it.  (Barrett:  Am.  Jour.  Obst.,  1914,  Ixx,  637.)  Correction  of 
surgical  conditions  of  the  pelvic  organs  often  are  followed  by 
improvement  in  the  goiter.  (Hertzler :  Jour.  Am.  Med.  Assn., 
1911,  Ivii,  2076.)  Cases  have  been  reported  by  Himmelhaber 
(Zentralbl.  f.  Gyiiak.,  1909,  xxxiii,  1225),  Leuf  (Am.  Me<l.,  1907, 
11.  s.  ii,  222),  Wells  (Med.  News,  1903,  Ixxxiv,  1209),  and  others  in 
which  simple  goiters  have  become  toxic  following  simple  opera- 
tions on  the  pelvic  organs.  I  have  experienced  two  such  calam- 
ities. It  is  interesting  to  note  that  the  relation  between  the 
genital  organs  and  the  thyroid  must  be  due  to  disturbance  of 
factors  other  than  inflammatory.  Acute  infections  of  the  geni- 
talia are  not  followed  by  thyroid  dysfunction.  Conversely,  it  is 
rare  to  find  a  thyroid  patient  who  has  pus  tubes.  In  the  ordi- 
nary toxic  goiters  the  ovaries  as  ductless  glands  seem  to  play  a 
relatively  slight  part.  In  the  forme  fruste,  however,  the  ovaries 
seem  to  be  more  closely  associated.  There  is  usually  a  pro- 
nounced dysmenorrhea.  Frequently  the  ovaries  are  very  small, 
wrinkled  and  contain  but  few  follicles.  These  findings  are  com- 
mon whether  the  patient  is  near  the  beginning  or  the  end  of  the 
menstrual  epoch.  The  sj^mptomatology  of  the  forme  fruste  is 
very  like  the  complaints  of  oophorectomized  women. 

Much  is  yet  to  be  learned  as  to  the  relation  of  the  sexual 
function  to  goiter,  but  the  interrelation  should  not  be  allowed  to 
rest  by  the  mere  statement  of  fact.  The  relation  should  be 
sought  for  in  each  case.    No  examination  of  a  goiter  patient 


20  niSEASES    OF    1HK    TlIVKOin    (ILAXn 

slioiild  1)0  regarded  as  coin])lete  without  an  exainiiiatioii  of  tlie 
generative  organs.  It  is  the  surgeon  \vlio  has  the  best  oppor- 
tunity to  develop  our  knowledge  along  this  line.  Now  that 
roentgenologists  liave  learned  to  castrate  w^omen  with  radium, 
we  have  a  new  material  in  which  we  may  study  the  loss  of  ova- 
rian function  on  the  nervous  system  and  the  thyroid  gland.  It 
may  also  he  noted  that  in  severely  toxic  cases  amenorrhea  is  by 
no  means  unconnnon. 

Some  of  these  cases  are  still  further  complicated  by  obvious 
signs  of  i^ituitary  disturbances.  Such  combinations  have  given 
license  to  the  expression  "polyglandular  disease"  wiiich  term 
has  liecome  the  synonym  of  all  that  is  weird  in  speculative  path- 
ology or,  i^erhaps  better  stated,  pathologic  speculation. 

Why  goiters  long  inactive  become  toxic  is  not  known. 
These  often  give  a  history  of  long  existent  simple  goiter  which 
show  no  evidence  of  toxicity.  Sooner  or  later  they  present  the 
usual  symptoms  of  thyroid  intoxication,  most  often  without  eye 
signs.  Very  commonly  pelvic  disease  of  a  character  requiring 
the  service  of  a  surgeon  is  found.  In  fact  it  is  uncommon  to  find 
such  cases  without  some  pelvic  lesion.  Not  uncommonly  this  type 
shows  toxic  symptoms  at  the  genital  involution  period.  This 
may  be  regarded  as  indicating  gonoidal  deficiency.  On  the 
other  hand,  often  the  signs  of  toxicity  do  not  appear  until  long- 
after  the  menopause.  This  makes  it  doubtful  whether  the  geni- 
tal lesions  so  often  found  play  any  etiologic  role.  If  they  do  not, 
then  we  are  forced  to  confess  that  we  have  no  clew  as  to  wdiy 
the  goiter  begins  to  cause  trouble.  Commonly  the  symptoms  of 
intoxication  develop  slowly  but  sometimes  the  onset  is  sudden. 

Heredity 

The  familial  occurrence  of  goiter  is  a  common  observation. 
AVhether  this  is  due  to  heredity  of  environment  or  a  biological 
heredity  is  another  question.  It  is  common  to  see  a  number  of 
members  of  a  family  affected.  I  have  had  the  grandmother, 
the  mother,  and  three  daughters  consult  me  at  the  same  time. 
They  came  from  a  goitrous  region.  Most  likely  heredity  plays 
a  prominent  part.  I  have  noted  numerous  instances  where  three 
or  more  daughters  became  goitrous  long  years  after  each  had 
left  the  parental  roof.    Not  infrequently  there  is  a  family  type 


ETIOLOGY    AXL)    PATHOGENESIS  21 

in  tliat  all  iiieinbers  affected  become  so  at  tlie  same  age.  Some 
families  do  so  at  an  early  age,  ^ay  below  fifteen,  others,  again, 
at  a  late  age,  say  after  thirty.  The  determination  of  the  ques- 
tion of  heredity  is  important.  If  the  mother  had  a  goiter  and 
it  disappeared,  there  is  better  prospect  that  the  daughters'  also 
will  disappear,  than  if  the  mother  got  hers  at  twenty  and  has  it 
still  at  fifty. 

In  the  forme  fruste  ty])e  thei-e  is  very  obvious  the  neurotic 
substratum  which  characterizes  the  type.  In  fact  frequently 
some  members  will  have  the  nervous  manifestations  without  any 
symptoms  that  can  be  ascribed  to  a  thyroid  disturbance.  These 
usually  suffer  from  ovarian  dysfunction. 

The   typical   exophthalmic   goiters   seldom   give   a  history 
of  numerous  cases  in  the  same  family  or  any  family  character- " 
istics  that  would  indicate  a  familial  predisposition,  either  or- 
ganic or  functional. 

Endemiology 

It  has  been  known  that  there  are  regions  in  which  goiter  is 
very  conunon  and  others  where  it  occurs  but  seldom.  Limestone 
and  lime-bearing  rocks  are  most  frequently  associated  with  en- 
demic goiters.  The  active  influences  were  for  a  long  time 
ascribed  to  geological  or  chemical  causes.  Bircher  (Ergebnisse 
der  Chirurgie  und  Orthopiidie,  Sprunger,  Berlin,  v,  133)  believed 
the  remains  of  extinct  flora  and  fauna  provided  the  noxious  ma- 
terial. These  regions  where  goiters  are  most  conunonly  found 
were  noted  to  be  mountainous  while  in  the  low  lying  regions  it 
was  less  frequently  observed.  This  does  not  apply  to  the  valley 
of  the  Arkansas  river  where  goiter  is  quite  common.  This  river 
contains  no  rock  and  but  little  water.  If  this  stream  is  culpable 
it  must  be  due  to  sand  and  sunflowers.  It  was  observed  that 
when  a  pure  or  at  least  a  difl'erent  water  supply  was  produced 
in  goiterous  regions  the  frequency  markedly  decreased.  Bircher 
(loc.  cit.)  notes  one  town  in  which  in  ]885,  59  per  cent  of  the 
inhabitants  had  goiters.  The  water  supply  was  then  obtainC'd 
from  another  source  and  in  1907  there  were  but  2i/2  P^r  cent 
goitrous.  It  has  not  been  satisfactorily  established  whether  the 
suspected  water  contains  a  deleterious  substance  or  lacks  some- 
thing essential  for  the  proper  functioning  of  the  thyroid.    Kim- 


22  DISEASES    OF    THE    THYROID   GLAND 

ball  and  Marine  (Arch.  Int.  Med.,  1918,  xxii,  41)  have  shown 
that  a  small  amount  of  iodine  will  prevent  the  development  of 
goiter  in  children.  Koclier  observed  that  those  who  drank  rain 
water,  though  living  in  goiterous  regions,  did  not  develop  goiter. 
Similar  observations  might  be  many  times  multiplied  from  the 
Swiss  literature. 

The  department  of  agriculture  has  determined  that  in  cer- 
tain regions  myxedematous  pigs  are  born.  When  food  from  a 
nongoitrous  region  is  fed  to  sows  in  regions  where  they  pre- 
viously had  farrowed  myxedematous  pigs  normal  pigs  are  born. 
This  indicates  clearly  that  the  disturbance  of  the  thyroid  is  due 
to  some  lack  in  the  food.  If  iodine  is  fed  to  the  pregnant  sows, 
normal  pigs  are  born.  It  seems,  therefore,  that  Marine  has  done 
the  same  service  for  the  human  race  that  governmental  machin- 
ery has  done  for  pigs. 

Infection 

Numerous  investigators,  notably  McGarrison  (The  Thyroid 
Gland  and  Its  Diseases,  Wm.  Wood  &  Co.,  1917,  p.  91)  have 
ascribed  the  influence  to  infectious  organisms,  probably  bacte- 
rial. He  sums  up  the  argument  in  favor  of  the  infection  theory; 
(1)  Goiter  decreases  in  prevalence  as  the  water  supply  increases 
in  purity.  (2)  Goiter  has  been  produced  by  injection  of  residue 
in  a  Berkefeld  filter  through  which  goitrigenous  water  has 
been  passed.  (3)  Exhibition  of  intestinal  antiseptics  causes  dis- 
appearance of  recent  goiters,  etc.  Adaini  (Montreal  Med.  Jour., 
1900,  xxix,  1)  had  previously  pointed  out  that  if  an  infection  is 
active,  it  must  be  of  a  peculiar  sort  because  it  comes  on  at  a 
particular  age  and  if  the  patient  removes  from  the  region  be- 
fore permanent  changes  occur,  the  goiter  disappears.  There- 
fore, the  infection  would  remain  operative  only  so  long  as  the 
patient  remained  in  the  goitrous  region. 

The  infectious  theory  led  naturally  to  the  search  for  foci  and 
the  teeth  and  tonsils  were  diligently  searched.  One  of  my 
former  assistants  (Dillingham)  followed  out  this  theory  with 
wholly  negative  results.  More  recently  influenza  has  been 
blamed  by  several  writers  and  a  number  have  been  observed  in 
this  clinic  who  dated  their  trouble  from  the  flu,  but  there  was 
no  evidence  obtainable  which  would  warrant  such  an  assump- 


ETIOLOGY    AXD    PATHOGENESIS  23 

tion.  Rlieumatism  and  tuberculous  infections  have  been  re- 
ported as  preceding  tlie  origin  of  tlie  goiter.  After  reviewing 
the  literature  designed  to  establish  the  infectious  character  of 
goiter,  one  can  readily  subscribe  to  the  statement  of  Professor 
Dock  that  ''Whether  sporadic,  epidemic  or  endemic,  the  cause 
of  goiter  is  unknown. ' ' 

Previous  and  Associated  Diseases 

Obviously  the  relation  of  a  chronic  disease  of  one  organ  to 
an  acute  affection  of  another  organ  is  difficult  to  determine. 
Many  authors  have  noted  the  appearance  of  goiter  soon  after 
the  patient  recovered  from  an  acute  disease.  Almost  all  the 
acute  diseases  have  been  mentioned.  The  tonsils,  of  course, 
were  at  one  time  vociferously  proclaimed  to  be  the  archenemy 
of  the  thyroid.  Be  this  as  it  may,  the  removal  of  the  tonsils 
does  not  appease  the  angered  thyroid.  Shurlenge,  however,  be- 
lieves that  he  has  seen  improvement  in  goitrous  patients  fol- 
lowing the  removal  of  tonsils.  Syphilis,  of  course,  has  been 
blamed.  Engel-Reimers  (Zentralbl.  f.  Cliir.,  1895)  has  observed 
a  swelling  of  the  thyroid  in  50  per  cent  of  cases  in  secondary 
syphilis.  Tuberculosis  also  has  been  blamed.  In  diseases  so 
common  as  goiter  and  tuberculosis  a  simultaneous  occurrence  in 
some  instances  must  be  expected.  It  has  been  assumed  that  the 
toxin  of  tuberculosis  acts  directly  on  the  thyroid  gland.  In  this 
region  where  tuberculosis  is  rare  it  is  very  exceptional  for  the 
diseases  to  coexist.  I  have  not  seen  such  a  case.  One  should 
not  be  too  hasty  in  assuming  a  relationship.  Moreover,  the  dif- 
ferentiation between  the  fruste  type  and  tuberculosis  is  the  most 
difficult  problem  the  student  of  goiter  encounters,  and  often  a 
diagnosis  is  not  possible. 

Neurogenic  Theories 

In  toxic  goiters  only  need  the  nervous  system  be  seriously 4 
considered  as  an  etiological  factor.  Because  of  the  symptom- 
complex,  exophthalmos,  tachycardia  and  goiter,  the  sympathetic 
system  was  early  considered  to  be  at  fault.  The  lesion  respon- 
sible could  not  be  decided  on.  The  exophthalmos  and  tachy- 
cardia appeared  to  be  due  to  a  stimulation  while  the  dilated 


24  DJSKASES    OF    THE    THYROID    GLAXl) 

vessels  of  the  tliyroid  could  be  explained  only  by  accepting  a 
paralysis  of  this  nerve.  Trosseau  met  this  difficulty  by  assum- 
ing a  neurosis  in  which  he  ])elieved  the  nerve  could  act  in  jDart 
as  an  excited  and  in  part  as  a  paralyzed  one.  The  vagus,  like- 
wise, was  accused.  The  lesion  hypothecated  was  a  pressure 
from  the  goiter  (Gros)  or  enlarged  lymph  glands  (de  Mussy). 
Others  liypothecated  a  lesion  in  the  medulla.  Many  attempts 
were  made  to  prove  this  theory  experimentally.  Other  centers 
Avere  experimented  with  but  no  investigator  has  succeeded  in 
producing  a  lesion  that  in  any  way  imitated  a  toxic  goiter.  That 
the  nervous  system  plays  an  important  part  cannot  well  be  de- 
nied, however.  In  the  typical  exophthalmic  goiter  there  is  in 
isolated  cases  a  definite  history  of  nervous  trauma.  In  these 
the  patients  relate  definitely  that  their  disease  began  following 
a  severe  nervous  shock.  I  recall  one  patient  whose  disease  fol- 
lowed a  fall  from  a  sidewalk  on  a  dark  night,  another  followed 
the  receijit  of  news  of  the  unexpected  death  of  her  mother;  one 
developed  after  being  struck  lightly  on  the  hand  by  a  wrench 
which  fell  from  the  top  of  an  oil  tower.  Mackenzie  related  a 
case  which  developed  following  the  meeting  of  a  drunken  man. 
A  generation  from  now  this  will  sound  more  j)lausible.  Clivostek 
presses  our  credulity  when  he  ascribes  one  case  to  the  discovery 
of  an  anal  fissure.  The  literature  is  replete  with  similar  in- 
stances. 

Crile  has  pointed  out  that  the  general  symi)tonis  of  toxic 
goiter  and  the  phenomena  of  fright  are  so  similar  that  they  may 
be  regarded  as  almost  parallel.  AVliy  in  some  instances  the 
phenomena  of  fright  continue  into  the  symptoms  of  the  disease 
has  not  been  explained.  Saying  that  metabolism  or  catabolism 
of  the  nerve  cells  is  increased  by  the  stimulus  of  the  excitement 
which  produces  a  toxic  substance  which  breaks  down  the  nerve 
cells,  thus  producing  a  vicious  circle,  sounds  plausible  but  no 
proof  can  be  offered  to  substantiate  it.  The  cases  in  which 
such  a  definite  relationship  to  nervous  shock  can  be  traced 
are  relatively  few  however.  The  onset  is  as  often  insidious, 
frequently  under  the  guise  of  intestinal  or  even  febrile  dis- 
eases. In  such  evidently  the  perverted  toxic  secretion  ante- 
dates the  disturbance  in  the  nervous  system.  These  cases 
which  develoj)  after  gynecological  operations  may  be  exjDlained 


ETIOLOCV    AXD    PATHOGENESIS  25 

either  as  a  nervous  traimia  or  a  disturbance  of  the  genital  func- 
tions or  both. 

AVe  are  yet  too  far  from  the  truth  to  be  able  to  define  the 
physiologic  relationship  of  psychic  trauma  and  toxic  goiter. 
Many  j)atients  have  a  suscepti))le  nervous  system,  but  many  do 
not  give  any  such  history.  The  defenders  of  the  neurogenic 
theory  contend  that  these  patients  remain  nervous  during  the 
remainder  of  their  lives.  There  is  much  truth  in  this,  but  it  is 
equally  trup  that  many  fully  recover. 

Thyrogenic  Theory 

It  is  easy  to  appreciate  the  arguments  in  favor  of  the  thy- 
]-ogenic  nature  of  the  disease.  Changes  in  structure  of  the  thy- 
roid gland  are  found  in  all  cases  of  toxic  goiter ;  by  the  removal 
of  a  part  of  the  gland  the  disease  is  favorably  influenced  and 
by  these  means  only.  These  statements  may  be  elaborated  with- 
out adding  strength  to  the  argument.  A.  Kocher  (Arch.  f.  klin. 
Chir..  19U,  xcv,  1007)  believes  that  the  varying  course  of  each 
disease  is  expressed  in  corresijonding  changes  in  the  histology. 
This  is  true  in  a  very  broad  way.  However,  the  severity  of  the 
disease  is  by  no  means  parallel  with  the  degree  of  anatomic 
change.  As  a  matter  of  fact  in  some  of  the  severest  cases  the 
gland  is  but  little  enlarged  and  the  histologic  changes,  while 
definite,  are  relatively  restricted.  In  many  the  removal  of  goiter 
tissue  is  not  followed  by  a  subsidence  of  the  symptoms.  The 
))lood  changes  noted  by  Kocher  (loc.  cit.)  are  not  always  pres- 
ent and  by  no  means  always  parallel  with  the  severity  of  the 
disease.  Furthermore,  in  the  degenerative  type  there  is  a  de- 
struction of  thyroid  tissue  without  in  many  instances  any  pro- 
liferation at  all.  These,  it  is  true,  may  be  excluded  from  true 
thyrotoxic  cases,  but  they  show  clearly  enough  that  the  prob- 
lem is  something  besides  over-production  of  thyroid  secretion. 

TJie  argument  that  like  changes  in  structure  may  occur 
without  any  toxic  symptoms  has  often  been  advanced.  It  is 
true  that  in  many  long  standing  goiters  one  finds  areas  of  epi- 
thelial proliferation.  Usually  in  such  cases  if  the  clinical  his- 
tory, the  blood  picture,  and  also  perhaps,  the  metabolic  rate,  are 
carefully  studied,  the  supi)osition  that  there  was  no  evidence 


26  DISEASES    OF    THE    THYROID   GLAND 

of  tliyrotoxicatioii  will  be  unsupported.  The  more  careful  the 
i^tudy,  the  less  common  are  the  disharmonious  observations.  The 
forme  fruste,  it  must  be  admitted,  often  shows  but  little  change 
in  the  gland  structure.  It  is  a  question,  however,  just  what  re- 
lation this  type  bears  to  the  typical  thyrotoxic  goiter.  One  may 
mistake  a  neurosis  for  a  forme  fruste. 

Likewise  the  argument  that  cases  of  thyrotoxicosis  are  ob- 
served without  any  specific  changes  in  the  colloid  falls  when  the 
gland  is  carefully  searched.  In  the  large  secondary  goiters  con- 
siderable search  may  be  necessary  before  one  finds  such  areas. 
It  cannot  be  too  much  emphasized  that  a  thyrotoxicosis  without 
changes  in  the  thyroid  gland  has  never  been  demonstrated.  The 
thyroid  gland  changes  are  the  one  constant,  demonstrable  factor. 

It  must  be  remembered,  too,  that  in  other  parenchyma- 
tous organs  there  is  also  a  variation  in  structure  as  compared  to 
function.  In  nephritis  one  sometimes  finds  marked  disturbance 
of  function  with  comparatively  little  structural  changes  to  ac- 
count for  them,  and,  conversely,  one  may  find  extensive  ana- 
tomic changes  with  a  relatively  normal  urine.  Yet  who  argues 
on  these  grounds  against  the  "'nephrogenic"  origin  of  nephritis  I 

We  may  gain  from  this  that  the  physiologic  and  the  ana- 
tomic so  far  as  our  crude  means  of  study  admit  of,  do  not  always 
run  parallel.  Or  in  other  words,  our  anatomic  knoAvledge  does 
not  enable  us  in  all  cases  to  gap  the  physiologic.  Then,  too,  the 
state  of  the  other  organs  may  in  a  measure  compensate  or  ag- 
gravate the  local  function.  The  adrenals,  as  well  as  the  thymus 
and  pancreas,  have  been  assumed  to  act  as  intermediaries  in 
magnifying  the  action  of  nerve  trauma.  The  action  of  the  adre- 
nals particularly  have  been  invoked  to  explain  the  action  of 
fright. 

On  the  other  hand,  the  evidence  in  favor  of  extraneous  in- 
fluences active  on  the  th3a'oid  is  largely  of  a  circumstantial  na- 
ture. These  are  all  more  or  less  subject  to  the  errors  incident 
to  the  personal  equation  of  the  observer.  The  most  commonly 
advanced  antagonistic  argument  against  the  thyrogenic  na- 
ture of  toxic  goiter  is  the  relation  of  nervous  shock  to  the  origin 
of  the  disease.  As  before  stated  instances  are  not  uncommon  in 
Avliich  the  disease  began  a  short  time  after  pronounced  nervous 
shock.    These  cases  are  so  numerous  that  it  does  not  seem  that 


ETIOLOGY    AXD    PATHOGENESIS  27 

coincidence  can  be  considered  in  the  argument.  If  the  nervous 
shock  is  the  primary  exciting  factor  how  does  it  bring  about  the 
anatomic  clianges  in  the  thyroid?  It  has  been  assumed  that  a 
vascular  dilatation  takes  place  which  results  in  the  parencliy- 
matous  proliferation.  There  is  no  evidence  for  this  because 
there  may  be  very  marked  proliferation  without  vascular  dilata- 
tion. We  may  assume  that  some  noxious  agent  is  liberated  by 
the  nervous  excitement.  Possibly  the  adrenals  perform  this  act. 
It  has  been  stated  that  grief  or  fright  may  cause  a  mother  to 
secrete  poisonous  milk  for  her  suckling  infant.  We  may  assume 
some  such  interaction  in  order  to  explain  the  changes  that  take 
place  in  the  thyroid  during  menstruation  and  pregnancy. 

When  all  the  factors  are  sifted,  one  does  not  get  beyond  the 
simple  fact  that  the  one  constant  factor  in  goiter  is  the  enlarge- 
ment of  the  thyroid  gland.  Surgeons  should  remember  that  the 
13athology  of  this  organ  does  not  explain  all  the  phases  of  the 
disease,  and  Avhile  removal  of  a  part  of  the  diseased  gland  does 
most  to  remove  the  symptoms,  it  is  fundamentally  unscientific 
and  the  endeavor  should  be  to  discover  the  fundamental  prob- 
lem in  its  etiology. 


CHAPTER  II 

NORMAL  AND  PATHOLOGIC  ANATOMY  OF  THE 
THYROID  GLAND 

In  an  organ  wliicli  is  normally  labile,  the  dividing  line  be- 
tween the  normal  range  of  variability  and  the  abnormal  must 
be  very  close.  It  seems  best,  therefore,  to  consider  both  in  the 
same  chapter. 

NORMAL  MORPHOLOGY 

Preliminary  to  an  appreciation  of  the  changes  that  occur  in 
the  diseased  thyroid  gland  it  is  necessary  to  understand  its  nor- 
mal structure.  Embryologically  we  may  remember  that  it  is 
formed  from  a  budding  out  of  the  areas  which  afterward  become 
the  pharynx.  Valuable  as  this  knowledge  is  in  enabling  us  to 
understand  the  various  aberrant  lobules,  it  is  of  no  aid  in  the  un- 
derstanding of  its  histology.  It  resembles  no  other  structure  in 
the  body,  and,  for  the  most  part,  comparisons  confuse  rather 
than  aid  in  the  understanding  of  its  formation.  Like  all  organs 
containing  cells  which  perform  a  specific  function,  it  is  made  up 
of  stroma  and  epithelial  parenchyma.  AVe  nmst  be  prepared, 
however,  to  see  the  epithelial  cells  present  a  variety  of  changes 
not  comparable  to  those  seen  in  any  other  organ,  because  it  has 
a  function  not  comparable  to  any  other. 

The  Capsule. — The  gland  has  a  thin  capsule  composed  of 
white  connective  tissue  (Fig.  1).  The  fibrils  are  flat  and  lami- 
nated. When  teased  apart,  large  ovoid  cells  are  seen  (Fig.  2), 
These  on  section  appear  spindle-form  but  when  the  cells  are  iso- 
lated they  are  seen  to  be  flat  with  ovoid  nuclei.  The  surface 
laminae  are  covered  by  a  more  or  less  complete  layer  of  such 
cells  (Fig.  3).  This  peritoneum-like  structure  accounts  for  the 
ease  with  which  the  gland  glides  about  under  the  overlying 
structure  on  movement  and  deglutition  and  also  for  the  facility 
with  ^vhich  it  reacts  to  irritative  changes  of  the  gland  paren- 
chyma.    It  contains  no  elastic  fibers  but  the  connective  tissue 

28 


XOIt^rAL    AXD    PATHOLOGIC    AXATOM  V  29 

lakes  Oil  a  glossy  refraction  like  that  of  the  peritoneum  imlieat- 
ing  an  elasticity  not  possessed  by  ordinary  connective  tissue 
and  permits  it  to  expand  to  meet  tlie  changing  requirements  of 
the  parenchyma. 

From  the  capsule  sustentacula  extend  into  tlie  interior  di- 
viding the  gland  into  more  or  less  distinct  lobulations  (Fig.  4). 
From  these  heavier  septae  liber  ])undles  extend,  forming  the 


Fig.    1. — Slide    of   a    normal    thyroid    gland    showing   the    thin    fibrous    tissue    capsule. 


-^^•^-i^aMi»-ji-Sf*;'^^;^iaa»«aV^r.i:!.,; 


K- . '  «.  ~sa.« 


Fig.    2. — ITigh    power    of    the    preceding   slide    showing   the    large    nucleated    cells    lying    between 
the    fiber   1)undles   which    compose  the   capsule. 

Avails  of  individual  acini.  These  terminal  fasculi  are  very  fine, 
being  composed  of  thin  bundles  of  reticular  tissue  (Flint:  Bull. 
Johns  Hopkins  Hosp.,  1903,  xiv,  32)  in  which  are  a  few  spindle 
cells  with  long,  narrow  nuclei.  In  most  places  it  forms  a  thin 
plane  of  tissue  on  which  the  cells  rest  (Fig.  5).  This  sustentacu- 
lar  tissue  has  much  in  common  with  tlie  subendotlielial  connec- 


30 


DISEASES    OF    THE    THYROID   GLAND 


Fig.    3. — Slide    of    a    normal    thyroid    gland    from    which    the    superficial    layer    of    the    fibrous 
capsule  has  been   teased   off  to   show   its   endothelial-like   character. 


Fig.    4. — Slide    of   a    normal    thyroid    gland    showing   the    septa    which    separate    the    gland    into 
secondary    lobules.     The    specimen    was    obtained    from    a    child. 


NORMAL   AXD   PATHOLOGIC   AXATOMY 


31 


1 


-    V 


Fig.   5. — Slide    showing    the    siistentacular    tissue    between     the    acini     teased    apart.     The     thin 
planes  of  tissue  with  small   spindleform  cells  are  shown. 


<i*« 


\    -^ 


•. 


J  '       ^ 


Fig.    6. — Cross    section     of    a    superior    thyroid    artery    just    below    the    surface    of    the    gland, 

showing  the   thick   walls. 


32 


DISEASES    OF    THE    TliYROlD    GLAXD 


tive  tissue  of  tlie  peritoiieiiin.  Tlie  uj^per  lamellae  are  covered 
by  cells  containing-  large  ovoid  vesicular  nuclei  very  similar  to 
the  endotlielial  cells  of  the  peritoneum.  They  do  not  seem  to 
differ  from  the  capillary  endothelium.  In  fact  there  is  no  sharp 
dividing  line  between  them.  Both  may  ])e  comjiosed  of  long- 
sheets  of  2oroto23lasm  like  the  capillaries  in  tlie  potential  vessels 
of  the  peritoneum  (compare  Hertzler:  The  Peritoneum,  i,  Fig. 
15,  p.  75). 


Fig.    7. — Injected    glain 


>\viiig    the    network    of    capillaries    in    the    interacinal    spaces    (^lajorX 


Blood  Vessels. — Because  of  the  great  vascularity  of  the 
thyroid  gland  the  study  of  the  circulation  has  received  consider- 
able attention  ])oth  because  of  its  theoretical  and  technical  in- 
terest. The  earliest  important  study  was  ])y  Baber,  (Philoi. 
Trans.  Eoy.  Soc,  London,  1876  and  1881)  and  Hiirthle  (Deutsch. 
med.  Wchnschr.,  1894,  xx,  267).  ^lore  recently  Major  has  stud- 
ied the  subject  (Am.  Jour.  Anat.,  vol.  ix,  -475)  and  has  also  col- 
lected the  literature. 

The  blood  supply  of  the  thyroid  gland  is  derived  from  su- 


XOR:\rAL    AXD    PATHOLOGIC    ANATOMY  33 

perior  and  inferior  thyroid  arteries  (to  be  described  in  the  eliap- 
ter  on  Anatomy).  They  form  a])undant  anastomoses  both  be- 
tween tlie  upper  and  lower  vessels  of  the  same  side  and  between 
those  of  the  o2)posite  side.  Major  dou])ts  that  there  is  anasto- 
mosis between  the  more  deeply  lying  arteries.  Experience  at 
the  oj^erating-  table  would  convince  one  that  they  inust  do  so. 
In  the  capsule  the  vessels  have  well  formed  walls  (P^ig.  6),  but 
these  rapidly  lessen  as  the  vessels  reach  the  interior  of  the  gland. 
As  soon  as  the  vessels  reach  the  gland  they  branch,  following  the 
septae  to  the  individual  acini.     Here  they  break  up  in  a  fine 


Fig.    8. — Slide    sliowing   a    superficial   vein    of   a    normal    thyroid    gland.     It    appears    as    a    broad, 
narrow   slit  just   below   the   capsule. 


capillary  network  which  surrounds  the  acini  (Fig.  7).  The  re- 
turn blood  is  taken  up  here  by  a  rich  plexus  of  veins  which  fol- 
lows tlie  septae  to  the  surface  where  they  are  collected  by  a 
complicated  plexus  of  veins. 

The  veins  are  characterized  by  their  delicate  walls  (Fig.  8). 
In  rapidly  developing  goiters  the  vein  wall  may  be  reduced  to 
a  few  fine  lamellae  while  in  old  goiters  the  walls  may  be  quite 
thick  due  to  the  proliferation  of  the  fibrous  tissue  walls.  The 
adventitia,  even  in  larger  ones,  is  very  sparse.  Their  tendency 
to  tear  on  manipulation  in  goiter  operation  is,  however,  due  less 
to  their  delicate  structure  than  to  the  reactive  changes  the  walls 
undergo  as  a  result  of  the  thyroid  changes.  According  to  Major, 
about  the  acini  the  capillaries  lie  just  outside  the  cells  in  the 


34  DISEASES    OF    THE    TliVKOlD    GLAXD 

connective  tissue.  The  capillaries  compared  to  the  cells  are 
very  large. 

L3niiph  Vessels. — The  lymphatic  circulation  of  the  thyroid 
gland  has  not  been  satisfactorily  worked  out.  According  to 
Baber  and  Petijean  (Bibliographie  Anat.,  xiv,  1905)  the  cai)il- 
lary  network  surrounds  the  acini  filling  the  interstices  between 
them.  These  collect  into  larger  trunks  in  the  capsule,  from 
Avhence  they  reach  the  lymph  glands  of  the  lower  cervical  region, 
and  in  addition,  according  to  Major,  one  trunk  passes  toward 
the  submaxillar}'  gland.  It  has  l)een  accepted  that  the  colloid 
is  absorbed  by  way  of  the  lymphatics,  but  Hunt  and  Seidell 
(Jour.  Pharmacol,  and  Exper.  Ther.,  1910,  xxvi,  32)  deny  the 
truth  of  this.  It  is  true  that  in  the  interacinal  connective  tissue 
clefts  may  be  seen  filled  with  colloid,  but  there  is  no  evidence 
to  show  that  these  clefts  are  connected  M'itli  the  lymphatic  sys- 
tem. On  the  contrary  the  cells  surrounding  these  colloid  masses 
are  indistinguishable  from  the  cells  lining  the  acini.  I  con- 
clude, therefore,  that  the  interstitial  cells  have  the  power  of  pro- 
ducing new  acini  and  what  has  been  mistaken  for  lymph  spaces 
containing  colloid  is  but  gland  formation  in  the  early  stages. 

Nerves. — The  nerve  supply  of  the  thyroid  gland  is  derived 
from  the  sympathetic  system  and  reaches  the  gland  through  its 
upper  pole  and  lateral  surface.  The  endings  have  been  traced 
to  the  acinal  cells. 

Acini. — The  acini  have  no  basement  membrane  in  a  true 
sense.  A  basement  membrane  has  been  described  by  some  his- 
tologists,  notably  Flint  (Bull.  Johns  Hopkins  Hosp.,  1903,  xiv, 
32)  but  unless  a  structureless  plasma-like  substance  which  ce- 
ments the  epithelial  cells  to  the  connective  tissue  stroma  be 
called  the  basement  membrane,  none  exists.  The  important  point 
consists  in  that  there  is  no  structure  which  resists  the  invasion 
of  the  surrounding  stroma  by  the  acinal  cells.  In  the  absence 
of  a  basement  membrane  the  thyroid  acini  resemble  the  uterine 
glands.  This  is  the  most  important  point  in  their  histology,  for 
it  is  dependent  on  this  fact  that  the  interacinal  connective  tissue 
becomes  so  readily  infiltrated  by  gland  cells  or  assumes  the 
morphology  of  acinal  cells. 

The  acini  are  variously  shaped  being  more  or  less  spherical 
or  polyhedral  (Fig.  9).    They  average  in  size  from  .3  to  1  mm. 


XORMAT.    AND    PATHOLOGIC    AXATOMY 


35 


Reconstniclioii  sections  aecordiiift'  to  Streiif  (Arch.  f.  Mik. 
Anat,,  xlviii,  579)  sliow  tlie  acini  may  be  irregularly  shaped 
with  various  accessory  pockets  and  interconinumicating  open- 
ings with  neighboring  acini.  The  colloid  contained  in  the  acini 
is  a  homogeneous  acidophilic  substance  which  stains  with  eosin 
about  the  same  shade  as  red  blood  cells.  The  similarity  is  most 
readily  seen  in  specimens  which  contain  blood  clots.  One  sees 
then  the  blood  ciot  and  the  acini  side  by  side.  The  colloid  in 
various  parts  of  the  gland  or  even  in  adjacent  acini  shows  varia- 


i/    /*■-<':•,•*'%.   .-/fV^v^',  ^l^X:!^i^-      . 


'^' 


,-^'*au> 


■*».  '.•'*• 


^    * 


Fig-.  9. — Slide  from  a  normal  thyroid  gland  showing  the  variation  in  size  and  form  of  the  acini. 

tions  in  staining  intensity.  The  colloid  is  attached  to  the  cells 
by  fine  jjrocesses  which  become  apparent  when  from  any  cause 
there  is  a  shrinking  of  the  colloid.  When  the  retraction  is  pro- 
nounced the  whole  border  is  serrated  or  dentated.  In  some 
glands,  supposedly  normal,  there  is  some  vacuolization.  This  is 
quite  constant  in  alcohol  hardened  specimens.  In  the  normal 
gland  there  are  a  few  empty  acini  when  frozen  sections  are  stud- 
ied, but  they  are  fewer  in  number  in  paraffin  slides.  The  colloid 
may  fall  out  during  the  manipulation  of  the  sections  in  any  tech- 
nic,  but  this  is  j^articularly  likely  to  occur  in  frozen  sections.  The 
more  careful  one  is  in  his  technic,  the  fewer  the  empty  acini,  so 


36 


DISEASES    OF    THE    TTrYP.OID    GLAXD 


it  may  l)e  tliat  empty  acini  indicate  only  rough  manipulation  of 
the  section. 

The  essential  cells  of  the  gland  line  the  acini.  Some  his- 
tologists  recognize  two  types  of  cells,  the  chief  and  the  colloid. 
Hiirthle  (Arch.  f.  d.  ges.  Physiol.,  1894,  Ivi,  1)  and  Langendorf 
(Biolog.  Centralbl.,  1880-90,  ix,  13())  nsing  Ehrlich-Biondi  stain, 
found  one  type  of  cell  which  stained  lightly  (the  chief)  and  the 
other  stained  deeply  due  presumably  to  the  contained  colloid. 
These  colloid  cells  are  probal)ly  but  the  functioning  stage  of  the 


€  \f^ 

^■jj^m-cffl 

i^     ^ 

Vr^Hj 

HB^^^^^^^^^^^^^^H          '  ■  ^y        ^1 

Fig-.    10. — High   power   of    the   preceding  showing  the   form   and   relation   of   the   acinal    cells. 

chief  cell.  These  cells  are  usually  described  as  being  cuboidal 
with  variations  between  the  fiat  and  columnar  (Fig.  10).  They 
are  not  comparable  to  cuboidal  cells  lining  the  acini  of  duct 
glands  in  that  they  are  more  irregular  and  the  intercellular  lines 
are  not  so  definitely  formed.  On  the  contrary,  the  protoplasm 
may  be  continuous,  forming  sj^ncytia-like  masses  resembling 
like  tissue  in  the  placenta  more  than  they  do  the  ordinary  type 
of  gland  epithelium.  In  a  state  of  compensatory  In^jertrophy, 
as  after  partial  resection  of  a  gland  and  in  pathologic  prolifera- 
tion, they  assume  a  more  pronounced  cuboidal  or  columnar  form 
and  may  then  be  compared  morphologically  with  the  common 


NORMAL   A^D   PATHOLOGIC    ANATOMY 


37 


type  of  gland  cells.  The  epitlielium  is  taller  in  young  subjects 
and  in  acini  containing  little  or  no  colloid.  Conversely,  in  old 
persons  it  is  more  flat,  and  in  nuicli  distended  follicles  in  goi- 
ters of  long  standing  the  endothelium  is  Hat,  closely  resembling 
endothelium  (Fig.  11).  The  nuclei  are  ovoid  with  vesiculated 
nucleoli.  In  old,  degenerated  glands  they  are  often  deeply  stain- 
ing with  little  evidence  of  vacuolization.  In  order  to  under- 
stand this  varying  ijliase  of  cell  morphology,  it  is  necessary 
to  study  the  teased  and  macerated  sections.     One  may  profit- 


Fig.  11. 


-Slide   from   an   old   colloid   goiter   showing  the   thin   interacinal   septae  and   the   low 
endothelial-like    acinal    cells. 


ably  study  the  structure  of  the  thyroid  by  treating  fresh  frozen 
sections  by  the  silver  nitrate  technic  commonly  employed  in 
the  study  of  the  peritoneum.  When  so  studied  the  irregularity 
of  the  cells  becomes  more  impressive.  The  intercellular  canalic- 
uli  described  by  Hiirthle  do  not  appear  with  this  technic. 
I  believe  they  ai-e  ai'tefacts. 

The  Interacinal  Cells. — Between  the  acini  are  regularly 
found  collections  of  cells  which  in  morphology  and  tinctorial 
reaction  do  not  differ  from  those  lining  the  acini  (Fig.  12). 
Their  constant  presence  and  great  variability  in  certain  types 
of  thyroid  intoxication  jjroclaim  them  to  be  elements  of  im- 


38 


DISEASES    OF    THE    THYROID   GLAND 


portance.  TIio  interstitial  cells  likely  differ  from  the  colloid 
as  the  Langhans  of  the  pancreas  differ  from  the  acinal  cells  of 
the  pancreas,  except  that  the  relation  is  closer  since  apparently 
the  interstitial  cells  may  under  certain  conditions  form  acini. 
These  cells  obviously  have  a  different  significance,  for  when 
these  are  in  the  ascendency,  the  symptoms  are  different  from 
those  when  the  acinal  cells  dominate;  when  both  are  damaged 
a  polyglandular  disturbance  results — all  within  the  thyroid 
gland. 

It  is  in  the  midst  of  these  interstitial  cells  that  masses  of 


Fig.    12. — Slide  of   a  thyroid   gland   taken   from   a   boy   aged   four   which   shows   the    interstitial 
cells  and  their  relation   to  the   acinal   cells. 

colloid  collect  and  from  these  new  glands  are  formed  (Fig.  12) 
much  as  new  vessels  form  in  adhesions  of  the  peritoneum. 
The  theory  that  the  accessory  acini  develop  from  preexisting 
acini  by  a  budding-out  process  does  not  seem  to  have  been 
demonstrated.  On  the  contrary  these  are  often  seen  in  old 
glands  in  which  the  acini  are  lined  with  flattened  atrophied 
epithelium  (Fig.  13)  while  the  small  glands  and,  from  the  tinc- 
torial reaction  presumably  new  glands,  show  nuicli  more  in- 
tense staining  reaction  (Fig.  13).  In  toxic  glands  in  which  the 
acinal  epitlielium  is  high  and  well  staining,  small  acini  in  proc- 


NORMAL    AXD    PATHOLOGIC    ANATOMY 


39 


ess  of  formation  can  be  traced.    In  these  it  is  sometimes  impos- 
sible to  distingnish  between  acinal  cells  and  interstitial  cells. 

It  is  im^Dortant  to  note  tliat  there  is  no  definitely  established 
normal.  Theoretically  we  may  assmne  that  the  thyroid  gland 
should  be  composed  entirely  of  acini  lined  with  a  single  layer 
of  cells.  As  a  matter  of  fact  such  a  simple  arrangement  ex- 
tending over  the  whole  gland  is  not  found.  In  some  areas  there 
is  a  piling  up  of  cells  in  the  interacinal  spaces  and  often  some 
papillary  formation  into  the  lumen.  Marine  and  Lenhart 
(Arch.  Int.  Med.,  1911,  xii,  506)   are  of  the  opinion  that  any 


Fig.    13. — Slide   from  a   slightlv  toxic   goiter    (interstitial   type)     showing  the   acinal   cells   inactive 
while   the   interstitial   cells  are   active. 


pajjillary  formation  is  an  indication  of  a  departure  from  the 
normal  state.  Naturally  in  human  material  these  points  are 
difficult  to  estal)lish,  for  operations  are  done  on  glands  sup- 
posedly diseased,  hence  the  specijuens  procured  are  supposedly 
abnormal  and  material  obtained  at  autopsy  is  natural!}^  obtained 
from  subjects  that  are  dead  sujjposedly  from  some  disease. 
The  latter  obviously  have  been  subjected  to  possible  changes 
due  to  the  disease  which  caused  tlie  death  of  the  patient.  Obser- 
vations of  value  on  this  point,  therefore,  can  be  obtained  only 
bv  the  study  of  thyroid  glands  obtained  from  bodies  in  which 


40 


DISEASES    OF    THE    TTfYROID   GLAND 


death  had  been  caused  by  violence  or  in  biopsy  material  ob- 
tained during  the  course  of  other  operations,  as  on  the  trachea 
for  tumors  or  strictures.  In  the  two  glands  obtained  after  vio- 
lent deaths  which  I  have  been  privileged  to  study,  neither  of 
them  was  "normal"  in  a  textbook  sense;  that  is  to  say,  many 
areas  showed  cellular  infiltration  of  the  interstitial  tissue  (inter- 
stitial cells)  and  some  indication  of  papillary  formation.  These 
changes  were  particularly  marked  in  the  slides  obtained  from 
the  gland  following  a  legal  execution.  It  may  be  argued  that  the 
mental  excitement  incident  to  the  traaric  end  mav  have  been  in 


Fig.  14. — Slide  obtained  from  a  boy  aged  four  years  made  from  tissue  removed  during 
an  operation  for  intratracheal  growth.  The  interstitial  cells  are  more  abundant  than  in  the 
adult   gland. 


part  responsible  for  the  changes  noted.  There  are  some  changes, 
however,  in  material  obtained  by  biops}'  Avhere  no  excitement 
has  existed,  or  at  least  no  more  than  might  be  excited  by  the  an- 
ticipation of  the  operation  and  during  the  exhibition  of  the 
anesthetic,  be  it  general  or  local.  Even  these  exciting  factors 
ai-e  absent  in  a  sudden  accidental  death.  In  all  such  tissues 
there  are  interstitial  collections  of  cells  and  such  complications 
nmst  be  regarded  as  within  the  range  of  the  normal. 

In  the  infant  and  in  young  children  the  presence  of  inter- 


NORMAL    AXD    PATHOLOGIC    AXATOMY  41 

stitial  cells  is  iiiucli  more  pronounced  (Fig.  14).  Tlie  epithelium 
is  piled  up  in  many  places  and  in  some  areas  there  is  a  lack 
of  lumen  extending  over  large  areas.  It  is  said  this  piling  up 
of  cells  in  the  acini  is  in  a  measure  a  compensator}^  process  and 
is  capable  of  being  influenced  b}^  diet  and  the  use  of  drugs.  The 
thyroid  organ  is  exceedingly  labile  in  its  function,  and  quite 
likely  in  some  of  the  wider  excursions  of  its  physiological 
responses,  structural  changes  as  well  accompany  them.  The 
rapidity  witli  which  changes  in  the  structure  of  the  gland  can 
take  place  has  been  studied  by  Marine  and  Lenhart  (Arch.  Int. 
Med.,  1909,  iv,  253).  They  describe  notable  changes  in  five  days 
and  complete  involution  in  twentj^-six  days. 

It  is  important  to  recognize  the  range  of  variability  of  the 
normal,  for  on  this  variable  normal  the  pathological  shades 
without  any  sharp  dividing  line,  giving  ample  reason  why  the 
normal  and  abnormal,  from  the  clinical  aspect,  is  so  hard  to 
determine.  All  the  available  evidence  must  be  concentrated  on 
the  question  of  normality  or  abnormality,  microscopic  study 
alone  is  not  sufficient. 


PATHOLOGICAL  ANATOMY 

In  a  malady  so  protean  as  goiter  there  is  always  difficulty 
in  correlating  the  physiological  and  pathological  changes  with 
the  clinical.  The  pathological  anatomists  at  best  can  but  study  a 
state  of  a  given  specimen.  It  is  only  by  studying  many  of  these 
with  constant  comparison  with  the  clinical  manifestation  that 
the  process  can  in  a  measure  be  charted.  In  goiter,  fortunately, 
most  of  the  tissues  offered  for  study  are  obtained  at  biopsies 
so  that  it  is  possible  to  compare  the  course  of  the  disease  before, 
with  that  after  the  tissues  are  removed.  Often  secondary  opera- 
tions furnish  further  material  for  the  study  of  a  given  case. 

The  study  of  such  material  makes  it  jiossible  to  divide  the 
pathology  of  the  thyroid  into  four  great  groups.  (1)  The  col- 
loid, in  which  there  is  an  accumulation  of  the  specific  secretion 
of  the  cells,  either  because  of  lessened  absorption  or  increased 
secretion.  (2)  Adenomatous  proliferation  including  increase 
in  the  activity  of  the  normally  situated  cell,  increased  intra- 
acinal  proliferation,  including  both  adenomatous  proliferation 


42  DISEASES    OF    THE    THYROID   GIAXD 

and  papillary  proliferation  of  the  acinal  cells.  (3)  Those  in 
which  the  changes  are  iDredoniinatingly  in  the  interstitial  cells. 
(4)  Degeneration,  including  degeneration  of  the  colloidal  con- 
tents, degeneration  of  the  acinal  cells  and  degeneration  of  the 
interstitial  connective  tissue.  These,  in  brief,  are  the  groups  in 
Avhich  the  inajority  of  goiters  may  be  placed  preliminary  to  a 
more  minute  study. 

Aii}^  combination  of  these  may  be  detected  in  a  single  speci- 
men. A  concrete  example  will  illustrate  this;  a  Avoman  of 
twenty -three  has  had  a  goiter  for  six  years.  Six  months  ago 
she  began  to  manifest  distinct  toxic  symptoms,  with  exophthal- 
mos. Four  weeks  before  operation  she  began  rapidly  to  lose 
weight  and  presented  other  evidences  of  extreme  toxicity.  The 
gland  shows  areas  of  colloidal  goiter,  albeit  with  some  evi- 
dence of  colloidal  degeneration,  distinctive  of  the  early  "inno- 
cent" stage  of  the  disease.  Other  areas  show  exquisite  papil- 
lary proliferation  distinctive  of  exophthalmic  goiter.  Finally 
other  areas  show  distinctive  degeneration  of  acinal  epithelium 
characteristic  of  the  extreme  toxic  state. 

The  adoi^tion  of  such  a  grouping  is  doubly  advantageous 
since  it  serves,  not  only  the  pathologist,  but  the  clinician  as 
well,  for  the  disease  as  he  sees  it  falls  into  one  or  the  other  of 
these  great  groups. 

It  is  well  for  the  surgeon  constantly  to  keep  in  mind  that 
there  is  no  sharp  dividing  line  in  pathology  any  more  than 
there  is  in  the  clinical  course.  He  should  not  expect  more  of 
the  pathologist  than  the  pathologist  may  expect  of  him,  an 
error  surgeons  habitually  make.  The  attempt  at  division  into 
certain  pathological  types  does  not  seek  to  provide  a  series 
of  hooks  upon  which  the  surgeon  can  hang  definite  disease 
pictures,  but  rather  to  aid  him  in  visualizing  the  changes  which 
have  occurred  in  a  gland  which  has  given  rise  to  certain  mani- 
festations which  he  of  all  others  must  be  most  able  to  recognize. 
Anatomic  study  is  of  less  A'alue  than  the  careful  clinical  obser- 
vation, but  the  surgeon  grasps  a  clinical  state  much  more  clearly 
if  he  can  visualize  the  anatomic  state  of  the  organ  he  contem- 
l^lates  attacking.  This  is  important  for  sometimes  the  more 
marked  pathological  changes  are  confined  to  certain  portions 
of  the  gland  and  the  surgeon  should  be  able  to  recognize  the 


XORA[AL    AXD    PATHOLOGIC    AXATOMY  43 

part  most  nearly  representing  tlie  normal  in  order  that  tliis 
may  be  preserved.  The  operating  room  diagnosis  is  as  impor- 
tant in  goiter  snrgery  as  it  is  in  the  operative  treatment  of 
tumors,  and  it  requires  as  much  careful  study. 

With  the  classification  of  goiters  as  already  mentioned, 
only  groujD  types  are  indicated.  AVithin  each  group  are  endless 
variations  which  can  be  comprehended  only  by  the  study  of  a 
large  number  of  specimens.  The  groujo  "carcinoma"  represents 
a  vast  variation.  The  appreciation  of  this  variation  becomes 
to  the  student  a  sort  of  subconscious  thing  to  be  employed  in 
his  clinical  work  but  which  he  is  not  able  to  express  in  abstract 
<liscussion. 

It  has  already  been  stated  that  the  majority  of  goiters  may 
be  i^laced  in  one  of  the  four  classes  already  mentioned,  the  col- 
loid, the  adenomatous,  the  interstitial  and  the  degenerative. 
This  holds  in  a  general  way,  both  for  the  laboratory  and  the 
clinic,  but  the  more  one  searches  for  detail  the  more  complex 
the  problem  becomes.  There  are  variations  in  the  clinical  pic- 
tures which  cannot  be  accounted  for  in  anatomic  stud}".  It  is 
l)ossible  that  this  variation  is  accounted  for  b}"  the  influence  of 
other  endocrine  organs  and  the  general  nervous  characteristics 
of  the  individual.  The  variation  is  no  greater,  however,  than 
we  find  in  carcinoma.  We  know  in  general  from  the  examina- 
tion of  a  given  tumor  what  the  nature  and  clinical  tendency  is, 
though  in  concrete  instances  they  may  surprise  us  in  the  rate 
of  their  growth  and  the  points  of  metastasis. 

In  goiter  more  than  in  any  other  disease  the  clinician  has 
to  do,  not  only  with  a  disease,  but  also  with  a  patient,  because 
general  conditions  react  so  constantly  against  the  thyroid  gland, 
that  not  to  study  the  two  together  is  not  to  study  the  disease 
at  all. 

Colloid  Goiter 

The  colloid  type  is  so -characterized  because  it  is  distin- 
guished b}'  an  increased  collection  of  colloid  in  the  acini.  The 
increase  of  the  colloid  present  may  be  due  to  an  increased  pro- 
duction or  a  decreased  absorption.  The  general  opinion  seems 
to  lean  toward  the  assumption  that  some  change  in  the  colloid 
takes    place    which    makes    it    less    readily    absorbable    than 


44 


DISEASES   OF    THE   THYROID  GLAND 


the  normal  colloid.  This  is  the  type  usually  found  in  early 
life  and  is  the  type  usually  observed  in  endemic  goiter.  I  am 
disposed  to  believe  that  the  picture  generally  accepted  as  that 


Fig.    15. — Section    of    a    small    recent    colloid    g-oiter    showing   the    uniform    granular    surface. 


Fig.    16. — -V    colloid    goiter    of    medium    size    showing    (a),    the    translucent    masses    of    colloid, 
and    (b),    the    mildly    bosselated    surface    showing   the    position    of    the    chief    colloid    masses. 


of  colloidal  goiter  is  really  that  of  a  resting  colloid  goiter.  In 
those  cases  in  which  operation  Avas  done  early  in  simple  cases 
there  has  always  been  evidence  of  cell  change.    As  a  matter  of 


NORMAL    AXD    PATHOLOGIC    AXATOMY 


45 


fact  no  developing  colloid  goiter  is  without  .some  evidence  of 
cellular  activity.  If  tlie  f)atient  is  carefully  observed  during 
the  period  of  rapid  development  some  increased  nervousness 
and  increase  of  pulse  rate  will  he  discovered  though  the  patient 


Fig.  i; 


-Section   of   a   large  colloid   goiter   of   long   duration   showing   degeneration 
with    secondary    hemorrhages. 


may  declare  herself  perfectly^vell.  When  the  gland  has  reached 
its  maximum  size  these  jdienomena  subside  and  the  gland  may 
remain  stationary  many  years  Avithout  producing  untoward 
syjni)toms. 

Gross  Pathology. — Colloid  goiters  usually  present  a  consid- 
erable increase  in  size,  frequently  both  lobes  are  nearly  uni- 


46 


DISEASES    OF    THE    THYKOID   GLAXD 


Fig  18. — Section  of  a  colloid   goiter,   of  45   years'   duration,   which   has   undergone 
extensive    fibrous    degeneration. 


Fig.    19. — Section    of    a   large    colloid    goiter    showing    uniform    enlargement    of    the    thyroid    lobe 
with   the  retention   of  the   original   lobulations. 


NORMAL    AND    PATHOLOGIC    AXATO.MY 


47 


foi'iiily  enlarged  l)ut  in  some  cases  one  lo])e  is  cliietly  enlarged. 
They  are  elastic,  soft  in  tlie  early  develoj)inental  stages,  firmer 
as  they  reach  the  resting  stage.  When  degeneration  takes 
place,   hemorrhages  may  take   place   into   their   snbstance   or 


Fig.  20. — Section  of  an  old  colloid  goiter  showing  the  unequal  development  of  the  lobules, 
(a)  Extensive  fibrous  degeneration;  (b)  calcareous  infiltration;  (c)  complete  degeneratien  of 
the  acinal  elements. 

cystic  or  calcareous  areas  may  sometimes  develop.  On  section 
they  are  deep  red  in  color  i)resenting  a  fine  granular  surface 
when  small  (Fig.  15),  paler  as  they  become  larger,  and  when 


48 


DISEASES    OF    THE    THYROID   GlJ^ND 


fully  develoi^ed  may  he  translucent  over  large  areas  (Fig.  16) 
with  lieinorrliagic  iiililtration  and  cyst  formation  in  older  goi- 
ters. Mass  degeneration  with  hemorrhage  usually  occurs  only 
in  those  which  have  attained  some  size  (Fig.  17).  Extensive 
fibrous  degeneration  (Fig.  18)  is  usually  seen  only  in  the  very 
old  ones.  In  some  of  them  the  original  lobulation  is  maintained 
(Fig.  19)  while  in  others  certain  lobules  develop  more  than 
others,  giving  rise  to  very  irregular  tumors  (P^ig.  20).  In  this 
way  secondary  lobules  may  extend  in  various  directions  beyond 
the  confines  of  the  goiter. 


Fig.  21.- — Slide  of  an  early  colloid  goiter  showing  the  uniform  increase  of  the  colloid 
without  changes  of  the  acinal  epithelium  or  retraction  or  vacuolization  of  the  colloid.  The 
interstitial   cells   show  no  activity. 


Histology. — In  the  average  run  of  colloid  goiters  there 
is  a  general  increase  in  the  colloid  differing  but  little  from 
normal  colloid  save  that  the  acidophilic  character  is  not  so 
uniform  (Fig.  21).  The  cells  are  not  notably  changed  in  the 
early  cases.  The  cells  are  fiat  or  cuboidal  and  stain  evenly  and 
remain  adherent  to  the  acinal  walls  (Fig.  22).  In  older  areas 
they  may  become  somewhat  flattened  while  still  retaining  their 
integrity.  The  cells  when  teased  from  their  acinal  walls  appear 
wholly  like  endothelium  (Fig.  1])  with  the  flat  ovoid  nuclei  and 


XOR.MAL    AXD    PATHOT.OGIC    AXATOMY 


49 


tlie  irregular  j^rotoplasmic  areas  between.    Still  later  tliey  suf- 
fer degenerative  changes. 

The  colloidal  increase  does  not  involve  all  acini  alike.  In 
some  areas  the  increase  may  be  so  marked  that  the  individual 
acini  are  visible  to  the  naked  eye.  In  others  there  may  be 
but  a  slight  or  no  increase.  In  some  apparently  simple  goiters 
there  is,  here  and  there,  some  vacuolization,  lack  of  tinctorial 
reaction  or  retraction  of  the  border,  factors  indicating  that  all 
is  not  well  in  the  gland.  In  some  there  may  be  considerable 
degeneration  in  the  colloid,  vacuolization,  retraction  and  tine- 


Fig.    22. — Slide    showing   the    flat,    inactive    cells    of    a   quiescent    colloid    goiter.      The    colloid 
shows    slight    vacuolization. 


torial  changes,  factors  ordinarily  indicating  a  toxic  degenera- 
tion, yet  there  are  apparently  no  clinical  symptoms  to  corre- 
spond to  these  changes  (Fig.  23). 

In  some  parts  of  the  gland  there  is  always  more  or  less 
increase  in  the  cells  in  the  sustaining  tissue.  In  some  of  them 
this  is  the  dominant  picture  (Fig.  24).  In  these  there  is  usually 
an  accompanying  nervousness.  These  cells  are  structurally  like 
those  lining  the  acini.  The  cell  clusters  may  form  lumens  and 
colloid  may  be  found  in  them  or  they  may  be  found  empty  after 
the  most  careful  technic. 


50 


DISEASES    OF    THE    THYROID   GLAXD 


Some  changes  in  the  cells  and  the  colloid,  suggestive  of 
pernicious  activity  can  be,  on  search,  found  in  the  most  ortho- 
dox and  innocent  colloid  goiter.  It  is  possible  that  these  cells 
may  in  some  waj^  injure  the  general  bodily  economy  though 
there  is  not  evident  any  definite  sign  or  deficiency  of  secretion 
or  absorption.  Myocardial  changes  are  most  often  found  asso- 
ciated with  goiters  which  show  changes  in  the  colloid. 

The  changes  in  the  vessels  are  often  marked.  There  may 
be  some  increase  in  the  size  of  the  interacinal  vessels  but  it 


.rm'f^ 


;'^r%«j3' 


X"- 


Fig. 


23. — Slide    from    a    clinically    inactive    Koiter.      The    colloid    is    markedly    redacted 
vacuolated.     The  interstitial  cells  show   some  activity. 


and 


is  not  marked.  The  chief  supplying  vessels  may  be  increased 
in  proportion  to  the  size  of  the  goiter;  I  have  seen  tlie  superior 
thyroidal  vessels  larger  than  a  normal  radial  at  its  origin.  The 
vessels  often  sIioav  extensive  atheromatous  degeneration,  a  fac- 
tor of  importance  in  ligation  of  the  vessels. 

There  is  a  type  of  goiter  seen  especially  in  girls  and  young 
women  in  which  there  is  no  notable  increase  of  epithelial  ele- 
ments but  which  is  associated  with  definite  toxic  symptoms. 
They  are  soft  and  turgid  but  not  tender.  The  changes  in  the 
colloid  are  exactly  parallel  with  the  changes  in  the  colloid  in  the 


XOR.MAL    AXD    PATHOI.OGIC    AXATOMY 


51 


socoiKlary  toxic  goiters  but  iiiiicli  less  marked.  The  colloid 
changes  its  reaction  to  dyes,  retracts  from  the  cell,  is  vacuolated 
and  in  the  more  pronounced  cases  the  colloid  contains  within 
some  destroyed  cells.  There  is  sometimes  round-celled  infiltra- 
tion. Aside  from  an  increase  of  the  pulse  rate,  there  is  little 
evidence  of  toxicity.  They  do  not  bear  iodine  and  its  adminis- 
tration may  produce  nervous  symptoms.  This  is  obviously  a 
close  approach  to  a  toxic  goiter  and  it  is  the  clinical  symptoms 
rather  than  the  microscopic  jjicture  that  enables  one  to  properly 
place  them. 


Fig.   24. — Slide     of     a     supposedly     inactive     goiter.      The     interstitial     cells     are     increased     antl 
there   has  been   absorption  of  the  colloid. 


Secondary  Changes. — As  already  noted,  it  is  only  in  the 
recent  goiters  that  the  simple  changes  chai^acteristic  of  colloid 
goiter  are  found.  In  old  glands  secondary  changes  are  numer- 
ous and  often  important,  and  may  be  regarded  as  representing 
only  the  normal  life  history  of  the  gland.  In  other  instances 
such  changes  take  on  added  importance  and  for  this  reason  re- 
quire special  emphasis. 

Cystic  Degeneration.— By  the  coalescence  of  a  number  of 
large  acini  a  veritable  colloid  cyst  may  be  formed.  The  con- 
tents may  be  predominantly  colloidal  or  a  variable  amount  of 


52 


DISEASES    OF    THE    TTIYKOID   GLAND 


lieniorrliage  may  liave  oceiirred  in  tlieni  (Fig.  25).  Sometimes 
tliese  cysts  containing  fluid  blood  are  ruptured  during  the 
course  of  the  operation.  The  sudden  appearance  of  so  large  a 
volume  of  blood  is  apt  to  scare  the  wits  out  of  the  young  oper- 
ator.   In  most  old  colloidal  goiters,  l)ecause  of  the  varying  de- 


Fig.  25. — Section  of  an  old  colloid  goiter.  To  the  left  at  the  bottom  of  the  figure  are 
lobules  developing  independently,  imitating  tetal  adenomas.  At  the  right  is  a  degeneration 
cyst  in  which  hemorrhage  occurred  with  disastrous  results.  At  the  very  bottom  of  the  ligure 
is    an    inverted    pyramid    of    nearly    normal    colloid    tissue. 


gree  of  hemorrhage  and  degeneration  that  has  taken  place,  the 
cut  surface  as  a  whole  presents  a  mottled  appearance.  Often 
too,  large  areas  of  gland,  interstitial  tissue  as  well  as  colloid  con- 
tents, may  undergo  degeneration  which  results  in  a  mass  of 


IsrORMAL    AXD    PATHOLOGIC    ANATOMY 


53 


structureless  gummous  material  which  escapes  if  the  gland  cap- 
sule is  ruptured  by  the  rough  manipulation  of  the  surgeon. 
These  secondary  cysts  when  small  may  be  lined  by  a  flat  epi- 
thelium which  in  many  instances  is  so  flattened  that  it  resembles 
the  endothelium  of  serous  surfaces  and  exhibits  a  tinctorial  re- 
action Avhich  characterizes  that  tissue.  More  often  the  epi- 
thelial lining  is  lost  and  when  there  is  nuich  degeneration  the 
Avail  is  made  up  of  tags  of  interstitial  sejjtae  in  a  greater  or  less 
degree  of  degeneration. 

Cysts  find  their  chief  practical   interest  in  that   extensive 


Fig.    26. — Sections    of    cysts    of    the    thyroid    showing    (a)     an    old    clot    indicating    an    ancient 
process  and   (b)   a  recent  hemorrhage. 


hemorrhage  into  them  may  so  increase  the  volume  of  the  gland 
that  the  trachea  may  be  suddenly  compressed  and  asphyxiation 
of  the  patient  occur.  AYhether  or  not  the  large  solitary  cysts 
found  in  otherwise  unchanged  glands  are  the  product  of  a  de- 
generative process  has  not  been  definitely  established.  Since 
they  are  usually  located  in  the  lower  poles  or  isthmus,  the  an- 
lage  likely  is  congenital.  Furthermore,  they  develop  progres- 
sively, indicating  that  they  are  neoplastic  in  character.  Hem- 
orrhage rarely  takes  place  in  them. 

Simple  cysts  are  among  the  rarer  tumors  of  the  thyroid 


54 


DISEASES    OF    THE    THYROID   GLAND 


gland.  They  usually  contain  a  straw-colored  fluid.  When  hem- 
orrhage takes  place  in  them,  the  fluid  is  red  and  it  may  coagulate 
after  removal  of  the  cyst  (Fig.  26-b)  or  the  clotting  may  take 
place  before  the  operation  is  done  (Fig.  26-a). 

Fibrous  Tissue  Degeneration. — As  this  type  of  goiter  be- 
comes older,  the  connective  tissue  may  become  markedly  in- 
creased.     So  great  may  this  become  that  whole  areas  appear 


Fig.  27. — Section  of  a  thyroid  showing  at  the  left  many  degeneration  cysts  which  collapsed 
during  the  operation,  and  at  the  right  the  more  recent  lobe  showing  beginning  colloid 
degeneration. 


niacroscopically  as  fibrous  (Fig.  27).  The  eijithelium  may  en- 
tirely disappear  or  become  degenerated  and  is  exfoliated  into 
the  colloid.  The  cells  may  become  pressed  together  and  because 
of  the  disappearance  of  the  colloid  they  appear  as  cell-nests  sur- 
rounded by  connective  tissue  (Fig.  28).  Such  areas  are  some- 
times regarded  as  malignant  by  credulous  pathologists.  As  a 
matter  of  fact,  if  tlie  niicroscopist  does  not  note  that  the  cells 
are  degenerated  and  that  the  iiln-ous  tissue  has  undergone  a  de- 


NORMAL    AXD    PATHOLOGIC    AXATOMY 


55 


gree  of  hyaloid  or  iiiyxoiiiatous  degeneration,  the  error  of  judg- 
ment may  seem  to  have  a  measure  of  justifieation.  Whether  the 
increase  in  connective  tissue  is  responsible  for  the  disappear- 
ance of  the  colloid  or  the  disappearance  of  the  colloid  is  fol- 
lowed by  increase  of  connective  tissue  cannot  be  stated.  As  a 
matter  of  fact  malignancy  does  not  develop  from  such  tissue. 
These  are  really  the  only  truly  ''innocent"  goiters.  When  the 
degeneration  involves  a  large  proportion  of  the  thyroid  tissue, 
a  hypofunction,  a  myxedema,  develops  despite  the  fact  that  the 
patient  has  a  goiter. 


Fig.  28. — Slide  of  a  goiter  which  has  undergone  fibrous  degeneration.  Below  is  shown 
the  degenerated  acinal  epithelium  with  increase  of  the  interstitial  cells.  Above  is  abundant 
fibrous  tissue  increase  compressing  the  cells,  giving  rise  to  a  superficial  imitation  of  a 
malignant  process. 


Calcareous  Degeneration. — In  very  long-standing  goiters, 
calcareous  deposits  may  form  in  or  about  degenerated  areas. 
Usually  the  deposit  forms  a  shell  in  some  part  of  the  tumor,  but 
complicated  partitions  and  septae  of  calcareous  material  may 
be  formed  (Fig.  29).  Sometimes  a  whole  lobule  may  become  en- 
cased in  a  lime  shell.  These  calcareous  plaques  not  infrequently 
become  attached  to  the  trachea,  making  separation  difficult  dur- 
ing operation  and  because  of  their  firnmess  may  cause  exten- 


56 


DISEASES    OF    THE    THYROID   GLAXD 


sive  erosions  of  the  tracheal  rings.  AVhen  these  plaques  extend 
over  the  upper  pole  upon  the  vessels  the  surgeon  may  feel  keen 
embarrassment  because  the  ligature  may  cut  through  the  ves- 
sel wall.  In  intrathoracic  goiter  the  unyielding  form  these 
masses  impart  to  the  goiter  may  make  operation  difficult  and 
hazardous.  Bone  formation  within  colloid  goiters  has  been  de- 
scribed.   In  many  of  the  reported  instances  the  description  is 


Fig.    29.- — Section    of  a   large   goiter   of   long  duration   showing   extensive   calcareous    degeneration 
which    at    the   lettered    points    forms    heavy    plates   of    stony    material. 


far  from  satisfactory  and  in  view  of  the  common  confusion  be- 
tween bone  and  calcareous  infiltration,  one  must  demand  a  care- 
ful histological  demonstration  of  bone  before  it  can  be  accepted 
as  such.    I  have  never  encountered  bone  in  a  thvroid.  A  number 


NORMAL    AXD    PATHOLOGIC    ANATOMY 


57 


rig.    30. — Slide    of    an    old    goiter    showing    activity    of    the    inters'.itial    cells    with    fibrosis    and 
secondary    hyaline    degeneration. 


Mll^-- 

*^* 

1 

J 

l^WKM 

Mi[i<'¥'^:|Pl^       MHH 

Fig.    31. — Slide    of    an    "innocent"    goiter    of    forty-five    years'    duration.     Carcinomatous    degen- 
eration   has   taken    place. 


58  DISEASES    07'    THE    THYROID   GLAXD 

of  uiKloubted  instances  have  been  recorded  by  Meyer  (Proc. 
New  York  Path.  Soc,  1919,  ii.  s.,  xix,  70)  Seahrt  (Centralbl.  f. 
Chir.,  1905,  xxxii,  337)  and  Pennel  (Lancet,  1917,  i,  454), 

Malignant  Degexeratiox. — As  already  mentioned  often 
the  fibrous  proliferation  causes  a  disappearance  of  the  acinal 
cells  or  they  may  be  so  distorted  that  malignancy  is  imitated. 
Sometimes  many  new  acini  form  in  such  tissue  Avhich  gives  the 
impression  that  they  are  invading  the  surrounding  tissue  (Fig. 
30).  It  is  questionable  whether  malignancy  ever  supervenes  on 
any  goiter  showing  secondary  fibroses.  Malignancies  in  my  ex- 
perience always  resemble  the  interstitial  glandular  prolifera- 


^i.?^*.!  '■^^^'^ 


Fig.    32. — Slide   of   an    adenomatous   goiter   which   caused    extensive    bone    metastasis.     This    slide 
was   made   from    tissue    removed    from   a  bone. 

tions  of  lumenless  acini,  and  it  is  such  areas  that  must  be 
scanned  for  dangerous  areas.  When  malignancy  occurs,  the 
cells  are  noted  to  be  larger  and  to  stain  more  deeply  and  form 
solid  masses  (Fig.  31)  or  the  acini  form  solid  cell  columi}s  (Fig. 
32).  Usually  the  thyroid  manifests  malignancy  by  active  acinal 
proliferation  and  not  as  a  scirrhous  or  even  a  simple  carcinoma- 
tous formation.  Therefore  the  consistency  of  the  thyroid  is  not 
of  the  same  value  in  the  determination  of  malignancy  as  it  is  in 
carcinomas  of  most  situations,  though  in  many  cases  the  consis- 
tency is  very  suggestive. 

As  is  well  knoA\Ti,  the  thyroid  may  exhibit  evidences  of  ma- 
lignancy witliout  showing  corresponding  structural  alteration 


NORMAL    AXD    PATHOLOGIC    AXAT0:MY  59 

and  the  thyroid  striit'tiire  may  be  easily  recognizable  in  the  met- 
astasis. On  the  other  hand  the  statement  that  metastases  may  go 
out  from  normal  glands  is  without  warrant.  There  are  ahvays 
changes  to  be  found  if  they  are  diligently  searched  after. 
Berard  and  Durnet  have  recently  (Eev.  de  Chir.,  1921,  xl,  521) 
collected  a  large  number  of  cases  and  have  come  to  the  conclu- 
sion that  in  none  of  them  was  the  thyroid  normal.  In  fact  to 
speak  of  the  metastasis  of  any  normal  organ  is  to  deny  the 
validity  of  our  fundamental  notions  of  malignancy.  The  met- 
astases are  particularly  likely  to  occur  in  bone  but  may  form 
secondary  nodules  in  any  tissue,  not  uncommonly  in  the  gut 
tract. 

Malignancy  is  diagnosticated  more  often  than  it  exists.  If 
the  patient  recovers,  the  gland  most  likeh^  was  not  malignant, 
yet  recoveries  are  often  reported  after  even  a  partial  removal 
of  the  gland.  The  surgeon  who  cures  a  carcinoma  of  the  thy- 
roid places  a  heavy  burden  on  his  pathologist.  If  ever  a  patient 
of  mine,  in  whom  a  diagnosis  of  malignancy  has  been  made,  re- 
mains well,  I  shall  renounce  the  diagnosis. 

Adenomatous  Goiter 

The  term  adenomatous  goiter  is  used  in  its  general  sense, 
that  is  to  say,  it  is  a  goiter  that  is  gland-like,  which  implies  that 
it  is  made  up  of  the  proliferation  of  the  acinal  cells.  Because  of 
this  active  jDroliferation  of  the  epithelial  elements,  this  type 
stands  out  in  marked  contrast  with  the  preceding.  In  colloid 
goiters  the  primal  disturbance  has  to  do  with  secretion  or  ab- 
sorption, while  in  the  adenomatous  type,  there  is  a  fundamental 
cell  multiplication.  As  one  might  suspect,  this  increase  in  cell 
elements  is  apt  to  be  attended  by  a  hyperfunction.  As  a  matter 
of  fact  this  phase  dominates  the  picture  clinically  and  the  term 
"adenomatous"  is  of  use  only  to  fix  the  attention  on  the  funda- 
mental anatomic  change.  Clinically  it  is  the  perverted  function 
of  the  proliferated  cells  that  fixed  attention  and  the  clinical 
synonym  is,  broadly  speaking,  thyrotoxicosis. 

There  are  certain  modifications  in  the  hypertrophy  which 
made  possible  a  certain  sub-classification.  (1)  The  fetal  adeno- 
mas in  which  definitely  encapsulated  areas  of  thyroid  tissue 
are  easilv  distinguished.    These  mav  or  mav  not  be  toxic.     (2) 


60 


DISEASES    OF    THE    THYROID   GLAND 


Tlie  diffuse  adenomas  in  which  more  or  less  of  the  wliole  gland 
is  involved.  The  glandular  proliferation  in  this  class  takes 
place  in  two  more  or  less  definite  directions;  (a)  the  one  shows 


Fig.   ZZ. — Photograph    of  a  fetal    adenoma   showing   its   smooth   ovoid   contour    and   the   unitorm 
fine    granular   character    of   the    cut    surface. 


Fig.    34. — Section    of  an    old    fetal   adenoma   which    has    undergone    complete    degeneration    with 
secondary    hemorrhage    and    cyst    formation. 


definite  multiplication  of  acini  producing  a  true  adenoma;  and 
(b)  the  other  in  which  the  epithelial  elements  pile  up  forming 
more  or  less  definite  papillary-  projections  into  the  lumen  of  the 
acini,  producing  a  papillary  adenoma;  and,  possibly  a  third 


XORMAL   AND    PATHOLOGIC    AXATOMY 


61 


group,  (c)  in  Avliieli  the  interstitial  cells  dominate.  It  may  be 
stated  at  the  ontset  that  broadly  speaking  Group  a,  corresponds 
with  toxic  goiters  without  exophthalmos;  b,  toxic  goiters  with 
exoi)hthalmos  and  possi])ly,  c,  to  the  forme  fruste  in  which  gen- 
eral neurotic  sym])toms  are  prominent. 

Fetal  Adenomas. — This  type  is  formed  by  a  comi^lete  encap- 
sulation of  a  portion  of  the  gland.    The  gross  appearance  pre- 


'*tf:*,0i^m0^ 


Fig.   35. — Slide    of   a    fetal    adenoma   showing   the    small    acini    with    little   colloid.     This    one    had 
recently  undergone  marked  increase  in  size. 


sents  an  ovoid  mass,  thoroughly  encapsulated,  which  permits  of 
easy  separation  from  the  surrounding  gland  tissue.  On  sec- 
tion the  gland  is  deep  red  and  finely  punctiform  (Fig.  33).  In 
rapidly  growing  types  colloidal  areas  may  be  detected  and  in 
old  regressive  areas  serous  or  hemorrhagic  cysts  may  be  formed 
(Fig.  3-1:).  The  structure  is  that  of  an  adenoma,  being  made  up 
of  closely  packed  glands  formed  of  small  cells.  The  colloid  con- 
tent is  very  small  and  may  be'  absent.  The  structure  indicates 
immature  development  closely  resembling  in  structure  the  gland 
in  the  fetus  (Fig.  35),  hence  the  name.  Ordinarily  these  acini 
contain  no  colloid,  but  when  toxic  sj^mptoms  develop  there  may 
be  a  variable  amount  of  colloid  present  (Fig.  36)  which  shows 
the  usual  changes  found  in  toxic  goiters.    Cellular  changes  are 


62 


DISEASES    OF    THE    THYROID   GLAXD 


not  eomnioii,  but  increase  in  number  of  acini  is  responsiljle  for 
the  gTowtli  of  the  tumor.  These  tumors  may  not  infrequently 
form  the  sole  lesion  and  their  removal  rids  the  patient  of  her 
disease,  but  as  often  a  general  glandular  hypertrophy  is  present 


Fig.  36. — Slide  of  a  toxic  fetal  adenoma  showing  the  presence  of  colloid  in  many  of  the 
acini.  At  the  extreme  left  of  the  figure  are  a  few  acini  of  the  adjacent  colloid  goiter.  A 
thin   capsule   divides   the    two   portions. 


Kig.    37. — Section    of   a    large    colloid    goiter    enclosing    within    itself   a    small    fetal    adenoma. 


and  the  adenoma  represents  but  a  part  of  the  disease,  and  is 
found  embedded  in  the  general  adenomatous  mass  (Fig.  37). 
Usually  these  tumors  are  solitary  and  are  easily  palpable.  When 
these  smaller  masses  are  discovered  with  the  microscope,  the 
examiner  is  apt  to  think  of  malignancy  (Fig.  38).    The  usual 


XORMAI.    AXD    PATHOLOGIC    ANATOMY 


63 


site  fo]'  tliese  adenonias  is  in  the  lower  pole  of  the  right  lo})e, 
less  often  in  the  isthmus  but  may  be  found  anywhere  in  the 
gland.  In  rare  instances  they  are  compound  tumors  being- 
formed  in  part  of  thymus  and  lymphoid  tissue. 


vi^ 


•'■—I  I 


>!^  .■  n 


l^j 


i^^M 


Fig.  38. — Slide  of  the  preceding  showing  the  structure  of  the  fetal  adenoniatuus  nodule  at 
the  left  and  that  of  the  colloid  part  to  the  right  of  the  picture.  Both  show  extensive  secondary 
degeneration. 


Fig.    39. — Section   of   a   recent   acutely   toxic  adenomatous   goiter    showing   fine   granular   appear- 
ance.     Its   dark   red   color   cannot   be   reproduced. 


Diffuse  Adenomatous  Goiters  (Glandular  Proliferations). — 

There  is  no  macroscopic  difference  between  the  glandular  and 


64 


DISEASES    OF    THE    THYrtOID   GLAND 


papillar\'  types.  They  vary  greatly  in  size  and  the  degree  of 
glaiididar  increase  bears  little  relation  to  the  severity  of  the 
intoxication  they  produce.  AVhen  small  they  may  be  firm  and 
elastic,  while  the  larger  ones  are  usually  soft  and  pulsating.  In 
many,  however,  and  these;  are  often  the  severest  cases,  the  gland 
is  very  firm  giving  the  general  feel  of  a  subacute  inflannnation. 
The  larger  ones  are  soft  in  the  ])eginning  and  tend  to  become 
firm  as  they  develop.  On  section  the  early  ones  are  red  with  or 
without  translucency  (Fig.  39).  The  older  ones  are  greyish  red 
and  may  even  have  the  color  of  boiled  liver  (Fig  40).     This 


'■     t 


Fig.  40. — Section  of  an  adenomatous  goiter  of  a  year's  duration.  The  fine  granular  sur- 
face within  distinct  lobules  is  shown.  Its  liver-like  consistency  and  grayish-red  color  cannot 
be    reproduced. 


change  in  color  presents  a  degeneration  of  the  interstitial  tissue 
as  well  as  of  the  colloid.  This  type  is  extremely  friable,  tearing 
on  the  least  tension,  making  ligation  or  suture  very  difficult. 
The  firm  areas  usually  show  some  reaction  on  the  surface,  as 
indicated  by  the  adhesions  between  the  gland  capsule  and  the 
surrounding  tissue,  which  likewise  adds  materially  to  the  tech- 
nical difficulty  on  their  removal.  The  endothelial-like  character 
of  the  superficial  layers  of  the  capsule  seems  to  facilitate  the 
development  of  adhesions. 


NORMAL   AND    PATHOLOGIC    ANATOMY 


65 


As  already  indicated,  glandular  proliferation  may  involve 
predominatingly  a  production  of  new  acini,  while  the  other  type 
presents  the  formation  of  papillary  epithelial  proliferation 
within  the  lumen  of  the  acini.  The  former  is  seen  in  the  toxic 
goiters  without  eye  signs,  Avhile  the  latter  is  characteristic  of 
the  classical  exophthalmic  goiter.  In  both  types  there  is  often 
a  diffuse  infiltration  of  the  interstitial  tissue,  with  gland  cells 
with  ovoid  nuclei  without  definite  gland  formation. 

The  Glandular  Type. — In  this  type  the  chief  change  is  in 
the  cells  lining  the  acini ;  they  become  higher,  stain  more  deeply, 


Fig.  41. — Slide  showing  a  typical  picture  of  to.xic  goiter  without  eye  signs.  At  o  the 
colloid  has  undergone  granular  degeneration  and  at  b,  it  has  disappeared.  At  the  right  of  the 
picture   there   is   marked   increase   of   the   interstitial    cells. 


and  x^resent  every  evidence  of  overactivity  (Fig.  41).  In  this 
type  there  is  also  a  marked  proliferation  of  the  acinal  cells  with- 
in the  interstitial  tissue  from  which  are  formed  secondary 
acini.  There  has  been  astonishingly  little  effort  made  to  deter- 
mine the  true  nature  of  the  cells  in  question  or  to  determine  the 
process  by  which  new  acini  are  formed  (Fig.  42).  These  sec- 
ondary acini  may  contain  little  or  no  colloid.  In  my  judgment 
it  is  a  mistake  to  confuse  the  interstitial  cells  which  are  found 
in  all  glands,  normal  and  abnormal,  and  the  round  cells  gen- 


66 


DISEASES    OF    THE    THYROID    GLAXD 


orally  recognizod  as  indicative  of  iiiflainination.  The  intersti- 
tial tissue  may  be  infiltrated  with  round  cells  and  in  some  in- 
stances these  become  so  numerous  as  to  simulate  lymphoid  tis- 
sue. Some  pathologists  have  even  described  germinal  centers 
in  such  areas.  In  my  judgment  these  are  not  germinal  centers 
but  represent  extensive  round-celled  infiltration  about  young 
acini. 

The  Papillary  Type. — In  this  type  there  is  a  proliferation 
of  the  cells  of  the  preexisting  acini  producing  tlie  projections 


Fig.  42. — Slide  of  a  toxic  nonexophthalmic  goiter  showing  the  development  of  secondary 
acini.  At  b,  is  a  well-formed  one,  at  o,  one  in  which  one  wall  is  made  up  of  interstitial  cells 
and  at  c,  is  a  space  containing  colloid  which  is  surrounded  by  interstitial   cells. 


of  papillary  formations  into  the  lumen  of  the  gland  (Fig.  43). 
This  is  the  most  constant  and  striking  picture  seen  in  the  study 
of  the  pathology  of  goiter.  It  is  distinctly  associated  with 
exophthalmic  goiter.  It  is  very  rare  to  find  eye  signs  without 
finding  the  characteristic  changes  and  on  the  other  hand,  these 
changes  are  often  found  when  no  eye  signs  can  be  demonstrated. 
In  this  type  more  than  any  other,  the  glands  present  evidence  of 
overactivity.  A  look  at  these  cells  suggests  at  once  the  idea  of 
overfunction.  When  the  papillary  formation  is  extensive  the 
picture  may  resemble  a  malignant  adenoma  (Fig.  44),  as  of  the 


XORMAL   AXD   PATHOLOGIC    ANATOMY 


07 


?T- 

1 

0^  ^ 

^^rst9^m^^ 

Fig.    43. — Slide    from    a    goiter    of    extreme    toxicity.     There    is    extensive    papillary    formation, 
but  the  interstitial   cells  are   also  much  increased. 


Fig.  44. — Slide  from  a  typical  exophthalmic  goiter.  There  is  extensive  papillary  formation 
with  but  little  participation  of  the  interstitial  cells.  In  some  of  the  acini  the  degenerated 
colloid  is  still  present. 


68 


DISEASES    OF    THE    THYROID   GLAXD 


fundus  of  tlie  uterus.  In  such  cases  there  is  usually  a  complete 
absence  of  colloid.  Where  the  proliferation  is  less  marked  there 
is  often  degenerated  colloid  (Fig.  45).  In  this  form  the  cells  are 
apt  to  be  high  columnar  and  deeply  staining  (Fig.  46). 

In  long-standing  cases  there  may  be  more  degeneration  than 
actual  proliferation.  This  is  noted  chiefly  in  those  cases  where 
the  acute  stage  has  long  passed.  The  cells  exfoliate  into  the 
lumen  of  the  gland  and  often  extensive  areas  become  degen- 
erated and  lose  their  ability  to  absorb  stains  (Fig.  47).  The 
colloid  if  any  is  present  is  degenerated  and  granular.    As  the 


Fig.    45. — Slide   from   a  goiter   in   which   the   eye   signs   developed   after   the   appearance   of   tlie 
toxicity.       The    paitillary    formations    project    into    the    degeneraied    colloid. 


degeneration  increases  they  come  more  and  more  to  resemble 
the  secondary  degenerated  eases  with  secondary  proliferation. 
In  extremely  toxic  acute  ckses  the  cells  are  exfoliated  giving  the 
appearance  as  if  the  slide  had  been  treated  with  some  destruc- 
tive chemical  (Fig.  48). 

Each  of  these  forms  of  active  cell  proliferation  is  com- 
monly associated  with  thyrotoxicosis.  While  there  are  no 
sharply  defined  lines  between  the  pathological  pictures  of  the 
various  types  of  intoxication,  one  may  predict  in  a  general  way 
from  the  clinical  symptoms  what  the  slide  will  show  and  one 


NORMAL   AND    PATHOLOGIC    ANATOMY 


69 


Fig.    46. — High    power   photograph    of    the    acinal    cells    of    an    exophthalmic    goiter.      They 
appear  as   tall  columnar   cells. 


Fig.    47. — Slide    showing    extensive    secondary    degeneration    in    a    primary 
toxic    adenomatous    goiter. 


70 


DISEASES    OF   THE   THYROID   GLAXD 


may  judge  from  the  slide  what  the  clinical  symptoms  and  prog- 
nosis may  have  been.  It  must  be  constantly  kept  in  mind  that 
all  parts  of  the  gland  are  not  equally  affected  and  one  may  find 
in  the  various  parts  of  the  gland  several  types  of  disease. 
Enough  of  the  gland  must  be  examined  to  insure  an  average 
picture  of  the  dominant  lesion.  The  more  thoroughly  the 
glands  are  studied  the  fewer  exceptions  will  there  be  to  this 
rule. 

Kecessions  in  toxicity  of  the  goiters  are  not  always  ex- 


^..C  i 


Fig.    Ai 


-Slide    sliowing    the    exfoliation    of    the    acinal    cells    in    an    acutely    fatal    case 
of  toxic  goiter. 


pressed  by  anatomic  changes  in  the  gland.  Usually  the  density 
of  the  gland  lessens  if  it  has  been  firm,  and  expansile  pulsa- 
tions cease  if  it  has  been  pulsating.  Probably  there  is  a  de- 
crease in  the  round-cell  infiltration  and  the  serous  exudate  in 
the  one  and  a  lessening  of  the  stimulation  of  the  vasodilators 
in  the  other.  This  inference  seems  warranted  because  of  the 
differences  observed  when  one  lobe  is  resected  in  the  stage  when 
the  goiter  is  firm  and  sensitive  to  pressure  and  the  other  re- 
sected when  the  remaining  lobe  has  softened  as  the  one  type  and 
in  the  other  there  is  a  lessened  vascularity  observed  at  the  op- 


XOKALAL   A:XD    PATHOLOGIC    ANATOMY  71 

eration  wlieii  the  oiJcratioii  is  clone  after  the  pulsations  liave 
ceased. 

In  order  to  make  the  pathologic  findings  harmonize  with 
the  clinical  observations  it  is  necessary,  therefore,  to  take  into 
account  the  stage  of  the  disease  as  learned  from  the  history  of 
the  case.  If  the  microscopic  findings  indicate  a  very  intense  in- 
toxication and  the  patient  does  not  present  evidence  of  it  the 
history  likely  will  reveal  that  the  disease  has  passed  its  peak. 

Glandular  Degeneration  (Secondary  Toxic  Goiter). — This 

condition  is  usually  implanted  on  a  long  pre-existing  colloid 
goiter  and  is  therefore  properly  called  "secondary  Basedow." 
Two  forms  may  be  distinguished.  In  the  first  there  is  a  gen- 
eral degeneration  without  reaction  either  on  the  part  of  the 
defensive  forces  of  the  body  or  by  proliferation  of  the  acinal 
cells.  In  the  other  type  there  is  a  proliferation  of  the  acinal 
cells  associated  with  the  general  degeneration.  One  may  call 
the  former  a  secondary  degenerative  toxic  goiter  and  the  latter 
a  secondary  proliferative  toxic,  being,  therefore,  not  strictly 
speaking  a  toxic  goiter  but  an  adenomatous  one  implanted  on  a 
pre-existing  goiter. 

Degenerative  Toxic  Goiter. — The  degenerative  type  should 
really  have  been  appended  to  the  degenerative  changes  in  col- 
loid goiter,  but  since  it  is  attended  by  grave  toxic  symptoms  it 
adds  to  clinical  clarity  to  discuss  it  here.  In  this  type  the  onset 
of  toxic  s\Tnptoms  is  usually  sudden,  occurring  chiefly  in  old 
women.  After  being  for  many  years  the  serene  host  of  an  ' '  in- 
nocent" goiter  the  patient  rapidly  loses  w^eight  and  becomes 
nervous.  The  gross  appearance  does  not  differ  from  old  col- 
loid goiters.  They  may  show  any  of  the  types  of  secondary  de- 
generation mentioned  under  that  type.  The  chief  changes  are 
usually  found  in  the  colloid.  The  gross  changes  are  those  of 
any  long  existing  colloid  goiter.  Even  Avhen  toxicity  is  ex- 
treme, the  gland  remains  firm  but  may  be  sensitive.  It  has  no 
pulsation  of  its  own  but  may  throb  with  the  much  excited  caro- 
tids. That  part  of  the  gland  responsible  for  the  intoxication  is 
the  part  which  previously  approached  the  stationery  colloid 
goiter.  Those  portions  which  have  previously  undergone  the 
usual  degenerative  changes  of  colloid  goiter  do  not  seem  to  take 


72 


DISEASES   OF   THE   THYROID   GLAND 


part.  The  colloid  shows  marked  vacuolization  (Fig.  49.).  The 
colloid  is  granular  and  is  largely  indifferent  to  any  stain.  It  us- 
ually shows  complete  retraction  from  the  acinal  cells.  The  cells 
show  a  lessened  tinctorial  reaction,  are  often  flattened  and  some- 
times are  loosened  from  their  basement  membrane  (Fig.  50)  or 
may  lie  free  in  the  colloid  substance  (Fig.  51).  In  these,  large 
areas  of  gland  sometimes  seem  to  have  undergone  necrobiosis. 


Fig.    49. — Slide   showing   degeneration    of   the   acinal   cells   and    the   colloid    in    a   secondary- 
toxic   goiter. 

This  same  process  ma}^  begin  in  a  thyroid  not  previously 
enlarged  or  in  the  jDortion  of  gland  remaining  after  a  partial 
lobectonw.  That  the  symptoms  are  due  to  dysfunction  is  sug- 
gested by  an  autopsy  Halsted  (Johns  Hopkins  Hosp.  Eept.,  1896, 
i,  373)  made  on  a  dog  in  which  a  complete  removal  of  the  thy- 
roid was  done  a  year  previously.  This  dog  became  emaciated, 
Aveak,  and  lost  its  hair  during  the  year  following  the  removal  of 
the  thyroid  gland.     Following  thyroidectomy  there  may  be  a 


NORMAL   AND   PATHOLOGIC   ANATOMY 


73 


t  ^'    '^ 


^%ll^ 


>♦ 


V, 


iff 


*- 


.% 


•■*ii^ 


.#  »*>  ,  l'^  •  ^ 


> 


^    ■% 

-# 

»^-^*     </ 


^*C     ST 


i 


Fig.    50. — Slide   showing   separation  of  the  acinal   cells   from   the   connective   tissue   in   a  second- 
ary  toxic    goiter. 


a^*^« 


I'ig.    51.- — Slide    from    a    secondary    to.xic    goiter    showing    the    acinal    cells    in    the    midst    of    the 

colloid   substance. 


74 


DISEASES    OF    THE    THYROID   GLAXD 


return  of  tlie  symptoms  of  tremor,  rajjid  pulse,  rapid  loss  of 
weight  and  death,  yet  at  autopsy  there  may  be  all  but  a  com- 
plete loss  of  all  thyroid  gland  tissue.  In  severely  toxic  cases 
with  increase  of  the  gland,  the  enlargement  may  disappear  and 
a  fatal  issue  ensue  without  any  change  in  symptoms  though  the 
gland  undergoes  complete  disintegration.  There  is  nothing  in 
our  present  theory  of  things  to  explain  this  extreme  anatomic 
variation. 

Secondary  Adexomatoits  Goiter, — This  foi-m  usually  occurs 
in  younger  women  than  the  preceding.    The  metabolic  changes 


Fig.    52. — Slide    from   a   secondary    toxic   goiter    showing   the    rejuvenescence    of    the    acinal    cells. 
The  colloid  has  undergone  extensive  granular  degeneration. 


are  less  pronounced  and  the  ordinary  symptoms  of  toxic  goiter, 
even  to  the  eye  signs,  may  be  noted. 

The  gross  sections  of  this  form  also  are  often  those  of  an 
ordinary  colloid  goiter  with  the  secondary  changes  this  type  is 
prone  to  undergo  if  long  existent.  In  persons  who  have  had  an 
"innocent"  goiter  many  years  all  the  secondary  changes  inci- 
dent to  colloid  goiter  may  be  found.  Often  the  goiter  is  very  firm 
and  sensitive  to  the  touch.  The  slides  do  not  show  infiltration 
Avhich  one  naturally  expects  to  find.  The  tenderness  evidently 
is  due  to  a  noncellular  infiltration.     Instead  of  there  being  a 


XORMAL   AXD    PATHOLOGIC    ANATOMY 


iO 


degeneration  of  the  cells  there  is  usnally  somewhere  in  the  gland 
a  rejuvenescence  of  the  cells  (Fig.  52).  Usually  the  acinal  cells 
are  increased  and  sometimes  there  is  an  increase  of  gland  forma- 
tion. When  exophthalmos  is  present  papillary  formation  will  be 
found  (Fig.  53).  In  this  type  there  is  often  more  or  less  round- 
cell  infiltration  in  the  connective  tissue.  These  areas  are  often 
so  pronounced  as  to  resemble  lymph  follicles  and  some  writers 
have  described  germinal  areas  in  them  as  was  described  for  the 
primary  adenomas.  The  coloid  is  vacuolated,  often  granular, 
and  frequently  contains  much  debris  of  epithelial  cells  as  de- 
scribed for  the  preceding  type.     The  retraction  from  the  cells 


Fig.    53. — Slide    from   a   secondary   toxic    goiter    showing    ijapillary    formation. 

is  apparently  the  earliest  and  mildest  change.  The  proliferation 
of  gland  acini  in  the  areas  where  gland  degeneration  is  the  most 
pronounced  gives  the  impression  of  a  compensatory  develop- 
ment of  gland  tissue.  It  is  not  a  normal  reaction,  however,  be- 
cause these  newly  formed  glands  do  not,  usually,  contain  colloid. 
These  hyperactive  cells  may  subside  and  the  goiter  again  as- 
sume its  "innocent"  state.^ 

In  this  type  of  goiter  sometimes  relatively  normal  areas  of 
gland  tissue  can  be  detected  at  the  operating  table.  These  areas 
are  commonly  found  near  the  upper  pole  and  to  a  lesser  extent 
at  the  lower  pole.  It  is  important  to  recognize  these  areas  at 
the  operating  table. 


76 


DISEASES    OF    THE    THYROID   GLAND 


Interstitial  Proliferative  Goiters  (Forme  Frusta) 

In  many  goiters  there  are  relatively  slight  changes  in  the 
acinal  cells  or  in  the  colloid  but  the  increase  in  the  cells  in  the 
interstitial  spaces  is  marked.  These  changes  may  consist  of  a 
mere  multiplication  of  these  cells,  sometimes  in  the  formation  of 
colloid-containing  spaces  resembling  young  acini.  The  acini 
are  but  little  enlarged  (Fig.  54)  and  the  colloid  but  little 
changed.  The  interstitial  cells  show  an  abundant  increase, 
widening  the  spaces  between  the  acini  quite  materially  (Fig. 


Fig.   54. — Slide    from   a   forme   fruste   goiter   showing   activity   in   the    interstitial    cells   with    little 
change   in   the   acinal   cells   or   in  the   colloid. 


55).  In  other  sections  large  areas  may  be  dominated  by  these 
cells,  the  acini  apparently  having  suffered  injury  by  compres- 
sion (Fig.  56). 

These  cells  do  not  differ  greatly  from  the  acinal  cells.  They 
differ  from  the  cellular  exudate  as  seen  in  inflammations,  but 
when  they  are  diffusely  scattered,  one  cannot  tell  when  the  in- 
terstitial cells  end  and  the  acinal  cells  begin.  This  is  sometimes 
seen  in  the  typical  Basedow  cases  of  a  very  acute  type.  This, 
however,  would  not  exclude  them  from  a  separate  category. 
Little  can  be  judged  of  a  cell's  function  by  its  appearance  as  an 


NORMAL   AND    PATHOLOGIC    ANATOMY 


77 


i 


Fig.    55. — Slide    from    a    forme    fruste    showing    marked    increase    in    the    interstitial    cells    with 
degeneration   of  the  colloid   substance. 


Fig.    56. — Slide    from    a    forme    fruste    showing    extensive    proliferation    of    the    interstitial    cells 
with    little    evidence    of    colloid    substance. 


78 


DISEASK.S    OF    TUE    TIIVROII)    GLAXD 


isolated  cell.  These  cells  do  not  represent  a  reactive  product 
for  in  glands  the  site  of  active  reaction  has  the  interstitial  tis- 
sue infiltrated  with  leucocytes  and  lymphocytes  {Fig.  57)  in  ad- 


Fig.     57. — Slide    from    a    I'oiiiu-    irii-^te    showing    on    the    left    of    the    figure    extensive    prolifera- 
tion  of   the   interstitial   cells   and    on   the   right   of   the   figure,    round-celled   infiltration. 


Fig.    58. — Section   of   two   cases   of   forme    fruste   shewing  the   fine    granular   surface. 

dition  to  the  interstitial  cells  but  these  present  the  classical  ap- 
pearance and  are  not  to  be  confused  with  the  cells  now  under 
discussion. 

The  source  and  significance  of  these  cells  is  an  unexplored 


XORMAL    AXD    PATHOLOGIC    ANATOMY  79 

field.  I  have  been  struck,  however,  with  the  very  constant  asso- 
ciation of  tliese  changes  with  the  forme  fniste  type.  Since  this 
tyjje  of  disease  differs  essentially  from  the  typical  Basedow  type 
it  appears  possible  that  the  thyroid  like  the  testicle  and  ovary, 
may  be  really  a  compound  gland,  the  interstitial  cells  represent- 
ing one  function,  the  acinal  cells  another.  If  this  were  true,  the 
thyroid  might  have  a  "polyglandular"  disturbance  all  by  it- 
self. The  thyroid  in  this  type  of  the  disease  is  small,  fine,  gran- 
ular (Fig.  58)  usually  firm  elastic  and  is  never  fragile  like  the 
true  toxic  goiters  often  are. 

Before  any  headway  can  be  made  along  this  line  the  his- 
tology and  histogenesis  of  the  gland  must  be  investigated  anew. 
That  colloid  in  the  interacinal  spaces  lies  in  the  lymph  channels 
has  not  been  proved,  and  that  this  material  is  the  product  of 
acinal  cells  and  found  its  way  into  the  interstitial  spaces,  either 
as  colloid  or  "precolloid,"  has  not  been  demonstrated. 

There  are  many  curious  and  inexplicable  mixtures  of  dis- 
turbances in  the  thyroid  gland  both  clinically  and  anatomically 
and  it  is  quite  possible  that  a  closer  morphological  study  may  re- 
veal much  of  interest. 

Pathology  of  Other  Org-ans  Associated  with  Goiter 

Unquestionably  too  great  a  proportion  of  attention  has  been 
centered  on  the  changes  within  the  thyroid  gland  and  too  little 
on  associated  changes.  This  finds  its  explanation  in  the  fact  that 
most  of  the  material  obtained  is  from  biopsies  and  in  the  second 
place  that  outside  of  the  thyroid  gland  there  is  little  or  nothing 
that  is  tangible.  Since,  however,  there  is  a  close  association  of 
the  thyroid  with  other  organs  this  very  fact  should  be  a  stimu- 
lus to  intensive  study. 

What  little  there  is  known  may  be  referreil  to  here  whicli 
at  least  is  impressive  in  its  paucity. 

Pathology  of  the  Nervous  System. — Surgeons  happily  have 
little  opportunity  to  study  lesions  other  than  those  of  the  tissue 
removed  at  operation,  hence  I  am  obliged  to  depend  on  the  re- 
corded autopsy  findings  of  the  internists.  The  most  constant 
finding  in  the  brain  is  petechial  or  larger  hemorrhages.  If  one 
remembers  the  usual  death  scene  of  these  cases  one  would 
hardly  wonder  at  this.    Klein  in  37  autopsies  found  fresh  hemor- 


80  DISEASES    OF    THE    THYROID   GLAND 

rliage  in  24  cases,  obviously  terminal  changes.  In  19  there  were 
changes  in  pons  and  medulla,  6  times,  in  the  cerebrum,  and  3 
times  in  the  cerebellum.  In  20  there  was  a  fresh  hemorrhage,  5 
times  a  leucocyte  infiltration,  3  times  fresh  degeneration,  in  2 
old  hemorrhages,  in  5  atrophy  of  ganglion  cells  of  the  fibre  bun- 
dles and  in  3  areas  of  acute  softening.  The  most  constant 
changes  are  in  the  medulla,  particularly  in  the  floor  of  the 
fourth  ventricle.  Hemorrhage  in  the  floor  of  the  fourth  ven- 
tricle may  be  responsible  for  the  terminal  hyperpyrexia.  Admit- 
tedly the  hemorrhages  are  recent  and  therefore  cannot  be  used 
as  explaining  causative  factors.  White  believes  there  are  pre- 
liminary changes  in  his  region  w^hich  may  be  softened  and  the 
hemorrhages  occur  here  because  of  the  previous  degeneration. 
Miiller  suggests  that  these  may  account  for  the  bulbar  symptoms 
sometimes  noted.  How  or  by  what  agent  these  areas  become  in- 
jured White  does  not  say. 

Crile  found  some  pronounced  changes  in  the  ganglion  cells. 
Wilson  (Jour.  Lab.  and  Clin.  Med.,  1917,  ii,  295)  has  described 
changes  in  the  sympathetic  ganglion.  He  notes  the  presence  of 
functioning  and  nonfunctioning  cells  in  immediate  proximity. 
Sucli  changes  are  not  found  in  patients  on  whom  a  complete 
lobectomy  has  been  done.  He  compares  the  changes  with  those 
seen  in  the  ganglion  cells  in  the  cord  in  poliomyelitis.  These 
changes  consisted  for  the  most  part  of  leucocyte  infiltration  and 
hyperemia  as  well  as  degeneration  of  the  ganglion  cells. 

The  findings  in  the  spinal  cord  and  peripheral  nerves  have 
been  even  less  impressive.  For  instance  Cheadle  found  hyper- 
emia and  White  some  isolated  hemorrhages.  Joffoy  and  Acliard 
found  slight  degenerative  changes  in  the  anterior  spinal  nerves. 

On  the  whole  it  may  be  safely  stated  that  the  pathologic 
changes  in  the  nervous  system  are  few,  inconstant,  and  unim- 
pressive. On  the  whole,  they  represent  terminal  changes.  They 
remind  one  very  much  of  the  autopsy  findings  in  cases  of 
eclampsia.  Those  who  argue  for  the  neurogenic  origin  of  thyro- 
toxicosis must  depend  on  clinical  observation,  for  no  anatomic 
confirmation  is  available. 

The  Thymus.— The  relation  of  the  thymus  to  toxic  goiter 
has  been  much  discussed.  Halsted  particularly  emphasized  the 
importance  of  a  careful'  consideration  of  this  gland.     On  the 


NORMAL    AXD    PATHOLOGIC   ANATOMY  81 

whole  it  may  be  said  that  in  recent  years  interest  has  lagged, 
perhaps  because  so  few  have  found  this  gland  enlarged,  either 
because  of  its  absence  or  of  faulty  technic.  Mikulicz  was  per- 
haps the  first  to  sound  a  word  of  discouragement.  As  a  source 
of  possible  danger  in  operative  prognosis  it  looms  larger.  Mc- 
Cardie  in  35  cases  of  sudden  death  in  goiter  patients  found  hy- 
perplasia of  the  thynms  in  18  cases.  Mackenzie  (Brit.  Med. 
Jour.,  1897,  i,  333)  in  1897  described  two  cases  of  Graves'  disease 
with  i^ersistent  thymus  and  (Am.  Jour.  Med.  Sc,  1897,  cxiii,  132) 
advised  the  use  of  the  extract  of  this  gland  as  a  therapeutic 
agent.  Capelle  thinks  there  is  a  persistence  of  the  thymus  in 
nearly  half  of  the  cases  of  Graves'  disease  and  is  present  in  85 
per  cent  of  the  cases  of  death  from  this  disease  and  in  95  per 
cent  of  cases  which  died  following  operation.  Slightly  lower 
figures  but  still  impressive  are  given  by  Schultze  (87  per  cent), 
Rehn  (87.5  per  cent)  Gebele  (80  per  cent),  and  Kocher  (60  per 
cent). 

That  the  thymus  is  not  a  direct  factor  is  attested  by  the 
fact  that  it  is  absent  in  a  considerable  number  of  cases.  The 
size  of  the  persistent  thymus  is  not  given  in  the  impressive  fig- 
ures above  quoted.  I  have  regularly  failed  to  find  the  gland 
for  reasons  not  clear  to  me.  At  any  rate,  the  very  large  glands 
mentioned  by  some  (Symmonds,  65  gm.,  Schlagerhaufer,  45-90 
gm.,  etc.)  have  not  been  present  in  my  patients.  It  is  possible 
that  the  enlargement  of  the  thymus  may  be  but  a  secondary, 
possibly  a  terminal,  process,  for  it  is  generally  believed  this 
gland  may  undergo  hyperplasia  in  infections  and  in  cases  of 
starvation. 

The  histologic  findings  likewise  are  inconstant,  or  at  least 
the  interpretation  of  them  is.  Most  authors  note  that  the  in- 
fantile type  is  retained.  Kocher  believes  a  medullary  hyper- 
trophy is  characteristic  of  the  Graves'  disease  thymus.  Schridde 
is  in  general  agreement  with  this.  Hassels  corpuscles  are  dimin- 
ished according  to  most  authors  but  according  to  Saupault  there 
is  a  marked  increase  and  Monckueberg  found  the  same  thing. 
Some  found  them  remarkably  large,  others  small.  Various  de- 
generations, notably  hyaline  and  calcareous,  have  been  noted. 
Fat    infiltration   has    been    observed   in    a   number    of   cases. 


82  DISEASES    OF    THE    THYROID   GLAXD 

Lymphatic  liypertropliy  lias  l)ccn  foiind  by  a  number  of  o))- 
servers.    It  is  a  rare  occiiiTence  in  my  experience. 

The  relation  of  hypertrophy  of  the  thymus  and  lymi^h 
glands  to  Graves'  disease  is  probably  that  of  general  intoxica- 
tion. The  great  variability,  and  the  inconstant  occurrence  pre- 
cludes the  possibility  of  a  direct  relationship. 

Suprajrenal  Gland. — The  changes  found  in  this  organ  seem 
to  be  irrelevant  for  the  most  part,  no  two  investigators  finding 
the  same  changes.  Kocher  found  hyperplasia  of  the  suprarenal 
when  there  was  hyperplasia  of  the  thymus.  Pettenvel  found 
lymph  follicles  in  two  cases.  Parode  found  proliferation  in  the 
medullary  portion  while  Pettenvel  found  a  hyperplasia  of  the 
cortical  portion.  In  one  patient,  who  died  in  this  clinic,  we 
found  the  suprarenal  capsule  generally  degenerated,  approach- 
ing a  state  or  necrobiosis. 

Hypophysis. — This  gland  has  been  but  little  studied.  Benda 
found  the  cells  small  in  all  portions,  while  Farners  found  a  gen- 
eral enlargement,  having  found  a  hyperemia  in  five  cases. 

Parathyroids. — McCallum  found  these  glands  unchanged. 
Humphry s  in  two  cases  found  an  infiltration  of  fat.  Stume 
found  tuberculosis  in  one  gland. 

Pancreas. — Askanagy  found  nothing;  Pettenvel  in  two  cases 
found  the  pancreas  atrophied  in  one,  in  one  an  atrophy  of  Lan- 
gerhans'  bodies  with  leucocyte  infiltration  and  areas  of  necrosis. 
In  coincident  cases  of  Graves'  disease  with  diabetes  the  char- 
acteristic pancreatic  changes  of  the  latter  were  found  by  several 
observers. 

The  Genital  Tract. — The  changes  in  the  genital  tract  co- 
incident with  goiter  are  numerous.  What  the  relationship  is  to 
goiter  is  another  matter.  The  changes  are  of  two  types,  those  of 
the  mid-child-bearing  age  in  which  there  are  lacerations  and 
displacements  of  the  uterus  and  in  the  adolescent  period  where 
there  are  hypoplasias.  The  former  are  associated  with  typical 
thyrotoxic  goiters,  while  the  latter  are  associated  with  the 
formes  frustes.  The  lacerations  and  displacements  and  other 
gross  surgical  lesions  cannot  have  a  direct  relation  whatever 
influence  they  may  have  on  the  nervous  system.  In  the  latter 
type  the  relation  is  such  that  a  direct  association  is  indicated. 
The  most  constant  finding  is  a  hypoplasia  of  the  ovaries.    The 


xor:mal  axd  pathologic  axatomy  83 

or^-aiis  are  small,  hard  and  contain  few  graafian  follides.  Often 
the  ntern.s  likewise  is  hypoplastic.  Hetzel  reported  a  case  in 
which  the  cervix  was  larger  than  the  body.  I  have  seen  several' 
such.  Pettenvel  found  the  ovaries  large  but  containing  few 
follicles  and  Farner  also  found  few  follicles. 

Circulatory  Apparatus. — From  the  symptomatology  of  toxic 
goiters  one  would  expect  extensive  changes.  Many  such  have 
lieen  reported.  For  the  most  part  these  consist  of  dilatation 
and  hypertroi3hy,  chiefly  of  the  left  ventricle.  There  are  con- 
siderable variations  noted  of  degree  and  combination  as  one 
might  expect  from  the  varying  duration  of  the  disease.  Various 
pigmentations  and  degenerations  of  the  heart  muscle  have  been 
noted  and  in  some  cases  marked  fatty  degeneration.  It  is  diffi- 
cult to  separate  out  lesions  due  to  some  pre-existent  disease  and 
those  due  to  the  goiter  itself,  if  such  there  be.  There  is  constantly 
an  increase  of  blood  pressure  sufficient  to  make  some  difference 
in  the  heart  muscle.  Possibly  the  increased  rate  may  add  to  the 
work-hypertrophy  if  it  is  such.  The  fact  that  there  are  de- 
generative changes  in  the  skeletal  muscles  makes  the  assump- 
tion plausible  that  there  is  some  direct  effect  on  the  heart. 

Digestive  Tract. — Collections  of  lymph  nodules  in  the  gut 
walls  have  been  noted  and  naturallj^  various  hyperemias  have 
been  observed. 

Liver. — Aside  from  congestion  and  fatty  degeneration,  few 
liver  changes  have  been  noted. 

Kidneys. — Hyperemia  and  degeneration  represent  the  few 
recorded  tindings.  The  changes  all  are  such  as  are  found  in 
the  usual  routine  autopsies. 

Muscular  System.— Askanazy  (Deutsch.  Arch.  f.  klin,  Med., 
1896,  Ixi,  118)  found  extensive  degeneration  in  the  skeletal  mus- 
cles. He  l)elieved  they  are  due  to  toxic  substances  circulating 
in  the  blood  vessels  and  have  nothing  to  do  with  the  nerves.  He 
found  the  degeneration  in  the  skeletal  nmscles,  diaphragm, 
esophagus  and  eye  muscles.  He  describes  the  changes  as  an 
interstitial  lipomatosis.  These  observations  have  been  con- 
firmed by  most  observers  but  a  few  have  failed  to  find  any  such 
changes.  A  possible  specific  relationship  is  rendered  doubtful 
by  the  fact  that  Langhans  found  like  changes  in  the  muscles 
of  cretins. 


84  DISEASES    OF    THE    THYROID   GLAND 

Osseous  System. — Osteomalatic  symptoms  liave  been  noted 
as  have  lymphocyte  infiltrations  of  the  marrow  of  some  of  the 
long  bones.  Unusually  thick  bones  of  the  skull  have  been  noted. 
The  known  relation  of  the  ovaries  to  osteomalacia  has  been 
used  as  an  argument  for  the  theory  of  direct  relationship  be- 
tween the  ovaries  and  the  thyroid  gland.  Be  this  as  it  may, 
there  is  nothing  in  the  pathology  of  the  bones  in  patients  dead 
of  goiter  to  give  it  weight. 

In  considering  the  findings  in  the  various  organs  above 
quoted,  it  is  interesting  to  note  that  most  of  the  general  findings 
are  such  as  might  be  accounted  for  by  the  fact  that  the  patient 
Avas  long  seriously  ill.  There  is  nothing  in  the  whole  category 
that  might  rightfully  be  ascribed  a  relationship  either  causative 
or  as  a  result  of  the  thyroid  change.  It  should  be  noted  that 
those  authors  who  find  changes  in  one  organ  find  changes  in 
many  other  organs,  while  those  who  report  negative  findings  in 
one  organ  do  not  find  anything  in  any  of  them.  The  suspicion 
is  raised,  therefore,  that  the  personal  equation  plays  a  consider- 
able role. 

General  Summary 

When  one  collects  the  opinion  and  observations  on  the 
pathology  of  the  other  organs  of  the  body  the  fact  remains  that 
the  only  definite  and  constant  pathologic  changes  are  found  in 
the  thyroid  gland  itself.  AVliile  the  variations  from  the  normal 
are  not  always  commensurate  with  the  clinical  symptoms,  the 
same  may  be  said  in  reference  to  the  kidneys  and  Bright 's  dis- 
ease as  Wilson  has  well  pointed  out.  The  variations  between 
the  normal  and  abnormal  are  very  close  it  has  been  noted.  The 
same  is  true  of  the  symptoms.  Transition  cases  occur  in  the  one 
as  well  as  the  other.  Kocher's  statement  that  a  normal  thyroid 
has  not  yet  been  demonstrated  in  a  case  of  goiter  still  holds. 
While  it  must  be  admitted  that  our  knowledge  of  the  pathology 
of  goiter  is  very  meager  and  unsatisfactory,  the  fact  remains 
that  what  Ave  do  knoAV  points  to  the  thyrogenic  nature  of  the 
disease. 


CHAPTER  III 

SYMPTOMATOLOGY  OF  DISEASES  OF  THE  THYROID 

GLAND 

The  clinical  signs  and  symptoms  of  goiter  are  so  protean 
and  the  dividing  line  so  narrow  that  it  seems  unwise  to  separate 
the  different  forms  in  treating  this  phase  of  the  subject.  It  is 
particularly  desirable  to  warn  against  the  complacent  regard 
of  any  goiter  as  simple.  There  is  no  simple  goiter.  One  had 
best  think  of  the  group  usually  considered  under  this  head  as 
not  yet  toxic.  Unless  one  does  this,  his  treatment  may  very 
quickly  convert  it  into  a  toxic  one.  In  harmony  with  this  view 
the  symptoms  which  may  be  found  in  any  goiter  will  be  dis- 
cussed in  turn.  This  is  eminently  practical  for  the  whole  list  of 
symptoms  must  be  considered  in  ev-ery  case  of  demonstrable  or 
suspected  goiter. 

Goiter 

An  enlargement  of  the  thyroid  gland  is  present  in  the  vast 
majority  of  patients  suffering  from  thyroid  diseases.  There 
are  rare  instances  in  which  the  gland  is  not  enlarged.  In  those 
instances  in  which  there  is  no  enlargement  there  can  always  be 
demonstrated  some  definite  anatomic  change.  In  every  case 
which  I  have  sectioned  there  have  been  distinct  changes,  wholly 
like  those  of  the  enlarged  gland.  There  may  be  a  thyrotoxicosis 
without  goiter  as  some  contend,  but  there  is  no  thyrotoxicosis 
without  disease  of  the  thyroid  gland.  Furthermore,  when  there 
seems  to  be  no  enlargement  to  palpation,  when  the  gland  is  ex- 
posed at  operation,  it  may  be  found  to  be  markedly  enlarged. 
Those  who  contend  that  there  are  patients  show^ing  the  thyro- 
toxic syndrome  Avithout  change  in  the  gland  have  yet  to  ex- 
hibit normal  glands. 

Degree  of  Enlargement. — Because  of  the  location  of  the 
thyroid  gland  there  is  no  satisfactory  method  of  determining 
whether  it  is  enlarged  at  all  or  not.     If  enlarged  there  is  no 

85 


86  DISEASES    OF    THE    THYROID    GLAXD 

scheme  wliereby  we  can  compare  it  with  the  size  of  other  glands. 
This  is  obvious  when  it  lies  substernally,  but  the  difficulty  may 
be  nearly  as  great  when  the  neck  muscles  are  well  developed 
and  the  adipose  deposit  generous. 

Ordinarily  in  average  necks  the  normal  thyroid  gland  is 
just  palpable  to  experienced  hands.  If  easily  palpable,  it  is 
probably  slightly  enlarged.  If  palpable  in  the  plump  patient, 
it  may  be  regarded  as  being  enlarged.  Often  an  increase  in 
consistency  is  as  valuable  as  evidence  as  increase  in  volume. 
Increase  of  sensitiveness,  likewise,  may  be  evidence  of  in- 
creased activity.  During  pregnancy  these  statements  must  be 
modified,  for  during  this  state  not  infrequently  the  thj^^roid 
gland  is  easily  palpable  in  the  normal  state. 

When  the  isthmus  is  present  it  is  usually  easily  detected 
lying  over  the  trachea  just  below  the  cricoid  cartilage.  The 
lateral  lobes  can  best  be  detected  by  placing  a  finger  on  either 
side  of  the  trachea  and  pressing  gently  downward  and  back- 
ward. This  is  usually  facilitated  by  inclining  the  patient's 
head  gently  forward.  If  the  patient  is  asked  to  swalloM%  the 
excursions  which  the  gland  makes  with  the  trachea  may  bring 
it  into  contact  with  the  examining  finger.  If  the  goiter  is  lo- 
cated behind  the  sternum  or  the  clavicle,  coughing  may  cause 
it  to  appear  or  to  transmit  an  impulse  to  the  examining  finger. 
In  the  latter  situation  the  x-ray  may  aid.  This  is  particularly 
true  if  the  goiter  is  an  old  one  which  has  undergone  fibrous  or 
calcareous  degeneration.  In  small  soft  goiters  the  x-ray  pic- 
ture may  be  unsatisfactory  or  misleading.  One  should  not  de- 
pend on  the  x-ray  examination  alone.  I  have  repeatedly  oper- 
ated on  patients  under  the  assurance  of  the  x-ray  man  that 
there  was  a  goiter  under  the  sternum  only  to  meet  disappoint- 
ment and  I  have  nnicli  oftener  operated  on  patients  whose 
chests  were  negative  to  x-ray  only  to  find  large  masses.  Both 
these  experiences  were  humiliating.  Percussion  also  in  large 
ones  gives  positive  evidence,  but  in  small  ones,  because  of  the 
bone  conduction,  this  method  too  leaves  one  in  doubt.  In  such 
cases  the  question  of  the  vocal  cords,  the  deviation  of  the 
trachea,  the  subjective  symptoms  must  be  taken  into  account. 
All  the  arts  known  in  the  diagnosis  of  mediastinal  tumors  must 
be  invoked. 


SYMPTOMATOLOGY  «/ 

Once  the  presence  of  goiter  is  determined,  a  means  of  com- 
parative record  is  desired.  There  is  no  satisfactory  way.  Men- 
suration is  unsatisfactory  because  of  the  varying  shapes  of 
necks.  It  is  impossible  to  place  the  tape  in  the  same  position 
each  time  a  measurement  is  taken.  Many  clinicians,  however, 
employ  this  method.  If  one  desires  to  depend  on  measurements, 
McGarrison's  scheme  (The  Thyroid  Gland  in  Health  and  Dis- 
ease, AVm.  Wood  Co.,  1917)  is  as  good  as  an5^  In  necks  measur- 
ing 13  to  16  inches,  he  assumes  an  increase  of  an  inch  repre- 
sents a  doubling  and  an  additional  increase  of  ^  to  %  a 
quadrupling  of  the  gland. 

My  experience  has  been  that  one  does  as  well  to  employ 
more  general  terms,  such  as  palpable  to  indicate  the  normal; 
easily  palpable  to  indicate  a  suspected  enlargement ;  small  when 
the  gland  is  the  size  of  an  egg ;  medium  when  the  size  of  a  tur- 
key egg,  and  large  Avhen  the  size  of  a  goose  egg.  For  the  very 
large  ones  usually  a  suitable  adjective  suggests  itself  when  the 
examiner  tirst  sees  it.  Usually  the  interne  attends  to  the  des- 
ignation in  a  satisfactory  manner. 

In  determining;  the  progress  or  regress  of  the  goiter  one's 
memory  is  as  good  as  a  measurement.  Men  and  elderly  women 
may  estimate  the  increase  or  decrease  by  the  tightness  of  the 
collar.  As  a  matter  of  fact,  the  size  of  the  gland  is  of  minor  im- 
portance, progress  of  the  disease  is  measured  better  by  other 
symptoms  than  by  the  size  of  the  gland. 

Consistency. — The  normal  thyroid  is  soft  and  elastic.  When 
it  is  enlarged  it  may  be  soft,  pulsating,  firm  or  even  hard.  Many 
early  large  toxic  goiters  are  very  soft,  almost  semi-fluctuating. 
As  they  grow  older  they  are  prone  to  become  harder.  The  toxic 
type  when  rapidly  developing,  when  soft,  is  usually  pulsating 
as  well.  The  pulsations  are  detected  by  placing  the  flat  hand 
over  the  goiter,  when  a  gentle  expansion  is  felt  with  each  pulse 
beat.  Expansion  must  be  distinguished  from  a  transmitted  im- 
pulse from  the  carotid  or  thyroid  arteries.  Colloid  goiters  when 
old  are  firm  and  when  firm  are  usually  sensitive  as  well.  This 
firmness  may  equal,  particularly  in  severely  toxic  cases,  the  feel 
of  cancer.  In  these  often  as  the  disease  subsides  somewhat  the 
hardness  gives  way  to  a  peculiar  liver-like  elasticity.  In  these 
cases  an  impulse  is  imparted  to  the  examining  finger  which  may 


88  DISEASES    OF    THE    THYROID   GLAND 

be  mistaken  for  expansion  of  the  goiter  but  it  is  due  to  the 
movement  of  the  whole  gland  in  response  to  the  impulse  of  the 
carotid  and  thyroid  vessels.  A  goiter  cannot  be  expansile  and 
hard  at  the  same  time.  When  fibrosis  has  developed,  par- 
ticulaily  if  calcareous  deposits  are  present,  bosselations  and 
angulations  of  positively  stone-like  hardness  are  felt. 

Sensitiveness. — The  normal  thyroid  and  the  colloid  goiters 
are  not  sensitive  to  ordinary  manipulation.  Toxic  goiters,  on 
the  other  hand,  are  often  sensitive  to  touch.  This  may  be  true 
when  the  gland  is  yet  too  small  to  be  positively  identified.  Se- 
verely toxic  goiters  are  often  as  sensitive  as  acutely  infected 
goiters.  In  these  very  sensitive  glands  the  subcutaneous  tissues 
may  be  somewhat  edematous. 

Mobility. — A  nontoxic  goiter  usually  is  freely  movable  un- 
der the  overlying  muscles.  Cysts  sometimes  are  so  mobile  that 
they  may  give  the  impression  of  lying  beneath  the  subcuta- 
neous fat.  Mildly  toxic  goiters  may  be  equally  mobile.  Those 
which  have  been  markedly  toxic  and  regressed  may  seem  mobile 
but  may  nevertheless  be  closely  attached  to  the  surgical  capsule. 
Acutely  toxic  goiters  may  be  so  firmly  fixed  that  they  are  but 
slightly  mobile  to  manipulation  and  follow  the  trachea  but  in- 
differently during  deglutition  or  more  correctly  speaking,  limit 
the  excursion  of  the  trachea.  The  importance  in  determining  the 
mobility  consists  in  that  thereby  the  difficulties  of  an  operation 
may  in  a  measure  be  judged.  In  a  measure  only,  for  not  in- 
frequently a  goiter  may  seem  freely  movable  and  yet  be  firmly 
fixed  and  present  mam^  difficulties  in  operation.  "\Mien  they 
are  firmly  fixed  the  problem  is  simple — the  operation  will  un- 
doubtedly be  difficult  and  the  surgeon  may  prepare  his  field  ac- 
cordingly. 

Aberrant  Goiters. — Goiters  or  parts  of  them  may  lie  at  sit- 
uations otlier  than  the  normal  places.  The  more  common  sites 
are  in  the  thorax,  at  the  angle  of  tlie  jaw  and  at  the  base  of  the 
tongue.     (See  Chapter  VI.) 

Eye  Symptoms. — It  is  the  symptoms  manifest  by  the  eyes 
that  distinguish  between  the  simple  toxic  goiter  and  the  ex- 
ophthalmic goiters,  or  true  Graves'  disease.  It  is  the  least  con- 
stant of  the  triad  of  symptoms  counted  as  pathognomonic  of 
Graves'  disease,  but  when  it  is  present  it  is  all  but  infallible. 


SYMPTOMATOLOGY  89 

The  eye  signs  are  present  in  less  than  10  per  cent  of  all  toxic 
goiters. 

Exophthalmia. — The  most  striking  of  the  eye  signs  is  prom- 
inence of  the  eyeball.  In  some  cases  other  eye  sjTnptoms  are 
present  withont  exophthalmos,  but  the  two  usually  go  hand  in 
hand  with  tlie  j)rotrusion  preceding  the  development  of  the 
other  signs. 

The  protrusion  of  the  eyeball  is  usually  noticed  by  the 
patient's  friends  before  a  physician  is  consulted.  Less  often  it 
appears  late  in  the  disease.  This  is  true  particularly  in  the 
degenerative  type.  In  mild  cases  the  expression  is  best  de- 
scribee! as  that  of  surprise  but  in  more  pronounced  cases  it  is 
more  that  of  terror.  It  is  never  that  of  anger  as  it  is  sometimes 
described.  The  facial  contour  of  the  patient  may  emphasize  or 
suppress  the  prominence  of  the  protrusion  and  the  degree  of  lid 
retraction  also  influences  the  apparent  prominence.  The  de- 
gree of  vascular  compensation  plaj^s  a  role.  When  there  is  de- 
compensation, it  may  be  increased.  Increasing  toxicity  and 
emaciation  may  act  in  tlie  same  way. 

Exophthalmos  is  bilateral  in  about  80  per  cent  of  the  pa- 
tients, but  one  side  only  may  be  affected;  in  such  instances  it 
is  usually  the  right  that  is  involved  and  not  infrequently  re- 
mains dominant  though  the  other  eye  may  protrude  later. 
Sometimes  the  most  prominent  eye  is  on  the  side  of  maximum 
thyroid  development  but  not  always.  The  degree  of  protrusion 
of  the  eyeball  varies  from  time  to  time  and  is  most  apt  to  be 
pronounced  at  the  menstrual  period.  The  cause  of  the  protru- 
sion has  been  discussed.  The  most  generally  accepted  expla- 
nation is  that  the  protrusion  is  due  to  the  contraction  of  the 
muscle  of  Miiller.  This  muscle  extends  in  the  upper  lid  from 
the  palpebral  insertion  of  the  superior  levator  palpebrae  muscle 
and  extends  to  the  tarsal  cartilage.  In  the  lower  lid  it  extends 
from  the  fovia  of  the  con.iunctiva  to  the  lower  border  of  the 
tarsal  cartilage.  Though  this  muscle  is  scarcely  1  cm.  in  length 
to  it  is  ascribed  the  power  of  giving  the  staring  look.  Schmitt- 
Eimpler  (Xothnagles  Handb.,  xxi,  1898)  denies  that  this  Aveak 
muscle  is  capable  of  producing  the  dislocation  of  the  eyeball. 
The  sympathetic  system  has  been  held  responsible,  presumably 
by  stinuilating  Miiller's  muscle  to  contraction,  and  to  counter- 


90  DISEASES    OF    THE    THYROID   GLAXD 

act  its  iiitiueiice  removal  of  the  superior  synipatlietic  ganglion 
has  been  advised.  There  seems  to  be  some  evidence  that  sec- 
tion of  the  sympathetic  is  followed  by  regression  of  the  eyeball 
in  some  cases.  The  operation  is  no  longer  done  which  may  be 
taken  as  evidence  that  the  previous  observations  were  erroneous 
or  that  the  results  are  uncertain  or  indefinite.  The  overfilling 
of  the  vessels  of  the  orbit  has  been  ascribed  an  important  part. 
The  fact  that  the  exophthalmos  disappears  after  death  has  been 
pointed  to  as  an  argument  for  this  theory.  Later  on,  no  doubt, 
the  orbital  fat  proliferates  and  adds  its  part.  The  evidence 
of  this  is  found  in  that  in  early  cases  the  prominence  of  the 
eye  can  be  reduced  by  gentle  pressure  while  later  on  this  is  not 
possible.  Earhardt  (Deutsch.  Chir.,  Lief.  38,  s.  232)  believes  the 
protrusion  is  facilitated  by  the  degeneration  of  the  ocular  mus- 
cles which  lessens  the  resistance  otTered  the  overdistended  ves- 
sels of  the  orbit. 

Exophthalmos  is  usually  the  last  symptom  to  disappear  af- 
ter cure  by  operation,  and  it  is  not  at  all  uncommon  for  it  to 
persist  to  some  extent.  This  persistence  may  be  ascribed  to  an- 
atomic changes  in  the  orbital  tissues.  Operations  have  been  de- 
vised for  the  removal  of  the  excess  fat,  but  the  results  do  not 
seem  to  warrant  imitation. 

The  degree  of  prominence  varies.  Sometimes  it  is  scarcely 
measurable  but  in  not  rare  instances  it  is  so  protuberant  that 
the  lids  do  not  close  and  in  very  rare  cases  the  eye  is  said  to  be 
actually  forced  from  its  socket.  A  number  of  instruments  have 
been  devised  to  measure  the  degree  of  exophthalmos.  They  can 
be  of  use  only  in  measuring  the  progress  of  a  case.  Since  there 
is  no  constant  relation  of  the  cornea  to  any  fixed  point,  it  can- 
not be  used  as  a  means  of  diagnosis.  When  the  exophthalmos  is 
so  great  that  the  lids  do  not  close  over  the  eye,  the  cornea  is 
nmch  endangered.  Jessop  (Ophthalmic  Review,  November, 
1895)  collected  25  cases  in  which  blindness  occurred  from  ulcera- 
tion. In  a  general  way  only  the  degree  of  exophthalmos  bears  a 
relation  to  the  severity  of  the  disease.  A  graphic  record  of  the 
degree  of  exophthalmos  is  difficult  to  obtain.  As  much  as  31 
mm.  protrusion  has  been  recorded,  usually  it  amounts  to  be- 
tween 5  and  20  mm. 

Imperfect    Movement    of   the    Upper    Lid. — Despite    the 


SYMPTOMATOLOGY  91 

marked  dis23lacenient  of  tlie  eyeball,  there  is  seldom  a  limita- 
tion in  the  range  of  movements  of  the  eyeball.  The  protrudent 
eyes  are  nsnally  symptomless.  The  eye  signs  other  than  those 
of  exophthalmos  have  to  do  with  the  movements  of  the  eyelids. 
They  are  usually  more  or  less  associated.  AVlien  one  is  present, 
the  others  are  quite  sure  to  be  sooner  or  later. 

Gra^fe's  Sign. — This  is  the  best  known  and  most  important 
of  the  eye  signs.  It  is  best  elicited  by  placing  the  finger  above 
the  horizontal  line  of  vision  and  after  the  patient  fixes  her  gaze 
on  the  finger  gradually  lowering  it.  It  is  seen  then  that  the  up- 
per lid  follows  the  downward  movement  but  imperfectly  and 
may  allow  an  area  of  sclera  to  appear.  The  lid  may  follow  the 
eye  downward  for  a  time  and  then  remain  stationary  while  the 
ej'eball  continues  its  journey  unattended,  or  the  lid  may  lag  be- 
hind but  follows  with  a  jerking  motion.  As  the  eye  is  moved  up- 
ward again,  the  lid  may  travel  the  faster  and  expose  a  consider- 
able area  of  the  cornea  until  the  eye  catches  up  and  then  the  two 
may  continue  upward  together.  It  has  occurred  several  times 
in  my  experience  that  when  the  patient  was  engaged  in  very  ex- 
citing conversation  so  that  his  attention  is  closely  fixed  and  in- 
terest excited,  one  or  both  lids  will  slowly  rise  exposing  a  rim 
of  cornea,  then  slowly  descend  again,  when  the  regular  tests  for 
von  Graefe's  sign  were  negative. 

A  pseudo-Graefe  symptom  may  be  present  in  some  cases 
Avhere  there  is  disturbance  in  the  innervation  of  the  eye  muscle 
due  to  some  central  nerve  lesion  as  in  Thompson's  disease  ana 
in  some  intrinsic  eye  diseases.  Orbital  tumors  may  cause  a  pro- 
trusion of  the  eye  and  a  Graefe  sign  may  be  simulated  so  far 
as  exposure  of  the  sclera  goes,  but  there  is  never  the  cogwheel 
movement  of  the  lid. 

The  cause  of  this  sign  has  not  been  established.  Contrac- 
tion of  Midler's  muscle  (Remak)  and  congestion  of  its  palpebral 
muscle  (Terry)  have  been  blamed.  Because  of  its  constant  as- 
sociation with  exophlhalmos  the  same  cause  likely  is  operative 
in  both  symptoms. 

Lessening  of  Involuntary  Winking. — One  of  the  earliest 
symptoms  is  that  first  described  by  Stellwag  (Wiener  Jalir- 
biicher,  1869,  xvii,  25).  It  consists  of  a  prolongation  of  the  in- 
terval between  involuntary  winking.    It  is  best  observed  when 


92  DISEASES    OF    THE    THYROID   GLAND 

the  patient  is  engaged  in  relating  her  history  or  when  the  exam- 
iner is  counting  her  pulse.  At  any  rate,  the  patient  should  not 
be  conscious  of  being  observed.  The  rate  of  normal  winking  as 
given  by  Stellwag  is  from  3  to  5  per  minute  while  in  Graves' 
disease  it  may  be  reduced  as  much  as  to  one  per  minute.  This 
s}Tnptom  often  gives  the  examiner  the  first  hint  as  to  the  na- 
ture of  the  disease.  It  is  associated  with  the  widening  of  the 
palpebral  fissure.  This  phenomenon  was  first  observed  by 
Dalrymple  and  first  recorded  by  W.  "White  Cooper  (Lancet, 
1849,  i,  551).  This  symptom  is  sometimes  observed  in  other 
nervous  diseases,  notably  in  hysteria.  The  excitement  incident 
to  the  first  meeting  with  the  examiner  in  susceptible  persons 
often  gives  these  nervous  patients  a  staring  look.  Even  this 
may  be  in  itself  an  important  sign.  If  a  person  accustomed  to 
meeting  strangers  stares  out  of  nervousness  it  should  suggest 
thyrotoxicosis.  On  the  contrary  rapid  blinking  may  occur  par- 
ticularly in  very  toxic  eases  especially  if  the  patient  has  learned 
of  this  eye  sign  from  previous  examiners. 

These  lid  S}Tiiptoins  are  seldom  present  when  there  is  no 
exophthalmos  but  in  some  instances  they  are  present  and  in  such 
cases  are  of  the  greatest  diagnostic  value.  They  are  by  no  means 
ahvays  present  even  if  exophthalmos  is  present  (Marie).  They 
sometimes  vary  from  day  to  day  being  present  sometimes  and 
absent  at  others,  or  are  present  in  varying  degree  of  prominence 
on  successive  days. 

Disturbance  in  Convergence. — Mobius  first  noted  the 
disturbance  in  convergence.  If  the  patient  is  asked  to  fix  his 
vision  on  a  distant  object  the  eye  is  unable  to  follow  it  to  as  near 
a  point  as  is  possible  in  the  normal  eye.  In  testing  for  this 
symptom  Mobius  advises  that  the  patient  be  told  to  look  at  the 
ceiling  and  then  quickly  at  the  end  of  his  nose.  One  of  the  eyes 
ceases  to  fix  the  object  and  turns  outward.  It  is  interesting  to 
note  that  double  vision  does  not  result,  but  the  patient  complains 
of  an  unpleasant  tension.  This  sign  does  not  maintain  a  rela- 
tionship to  the  signs  previously  mentioned  and  it  is  usually  not 
present  until  there  is  a  pronounced  exophthalmos.  This  symp- 
tom may  be  noted  in  nervous  affections;  is  one  which  can  be  used 
only  by  those  familiar  with  the  exact  examination  of  the  eye; 


SYMPTOMATOLOGY  93 

and  is  of  rolatively  little  importance  because  when  it  is  pres- 
ent other  more  characteristic  signs  are  easily  elicited. 

Uncommon  Eye  Signs. — Clifford's  Sign. — Gifford  (Ophtlial. 
Rec,  1906,  XV,  249)  described  a  symijtom  occasionally  present.  It 
consists  in  a  marked  difficnlty  in  everting  the  eyelid.  It  is  not 
due  to  a  thickening  of  the  tissues  but  to  a  spasm  of  the  levator 
muscle.  It  is  observed  early  and  tends  to  disappear  later  in  the 
disease.  It  is  a  curiosity  rather  than  a  symptom  of  much  diag- 
nostic value  because  when  it  is  present  the  other  symptoms  are 
pronounced. 

Pupil  Sign. — The  pupils  are  usually  not  affected,  occasion- 
ally one  pupil  is  larger  than  its  fellow.  This  is  usually  noted  in 
large  thyroids  which  press  on  the  sympathetic  nerves.  Occa- 
sionally patients  come  with  this  as  their  chief  complaint.  If  there 
is  any  disturbance  in  the  size  or  motility  of  the  pupil  some  other 
cause  should  be  diligently  sought.  The  reaction  to  light  is  nor- 
mal. 

Field  of  Vision. — In  some  instances  the  field  of  vision  is 
contracted  (Kost,  Wilbrand).  These  symptoms  may  be  due  to 
complications,  notably  that  of  hysteria  (Mobius). 

Tear  Secretion. — The  secretion  of  tears  may  be  nmcli  in- 
creased, even  to  such  a  degree  as  to  cause  the  patient  annoyance. 
On  the  other  hand,  the  conjunctiva  may  be  so  dry  as  to  greatly 
harass  the  i)atient.  Corneal  ulcer  is  a  rare  complication,  but 
^^  hen  it  does  occur,  is  a  serious  one,  and  not  infrequently  results 
in  the  loss  of  the  eye.  Liability  to  ulceration  does  not  run  par- 
allel with  the  degree  of  exophthalmos.  Some  of  the  most  pro- 
nounced degrees  of  ulceration  occur  in  cases  with  relatively 
slight  protrusion.  In  some  cases  there  is  an  anesthesia  of  the 
cornea.    This  may  predispose  to  ulceration. 

Nystagmus. — A  rare  sign  is  an  oscillatory  movement  of  the 
eyeball.  It  is  sometimes  present  while  gazing  in  certain  direc- 
tions.   Koclier  saw  it  only  in  a  few  instances. 

The  eye  signs  above  enumerated  are  all  but  pathognomonic 
of  thyrotoxicosis.  Usually  there  are  symptoms  which  Avill  per- 
mit a  diagnosis  without  tliem.  Too  great  emphasis  of  this  mem- 
ber of  the  triad  has  caused  many  cases  of  thyrotoxicosis  to  be 
overlooked.  On  the  other  hand,  obscure  cases  without  goiter 
are  sometimes  first  recognized  by  the  presence  of  the  eye  signs. 


94  DISEASES    OF    THE    THYROID   GLAND 

Involvement  of  the  Muscular  System. — The  voluntary  mus- 
cular system  is  affected  l)y  tremor  and  weakness.  The  former 
resembles  an  overstimulation  and  the  latter  a  loss  of  control 
of  the  nerve  supply. 

Tremor. — A  fine  tremor  of  the  hands,  less  often  of  other 
parts  of  tlie  body,  is  one  of  the  most  constant  s>iiix3toms  of  thy- 
roid intoxication.  Charcot  and  Pierre  Marie  seem  to  have 
'heen  tlie  first  to  emjDhasize  the  importance  of  this  symptom.  The 
latter  measured  tlie  rate  and  degree  of  the  tremor  by  means  of 
tracings  on  a  carbon  sheet.  He  found  the  rate  varies  from  8 
to  10  to  the  second.  He  discovered  furthermore,  that  the  normal 
individual  shows  a  very  fine  tremor  of  the  same  rate. 

The  tremor  is  often  observed  even  before  the  rapid  heart 
or  other  signs  of  thyroid  intoxication.  On  the  other  hand  it  is 
present  in  many  nervous  states  as  in  hysteria  and  neurasthenia 
and  in  alcoholic  tremor.  Generally  speaking,  in  nervous  states 
it  is  not  so  constantly  present  as  in  thyroid  intoxication.  On 
the  other  hand  it  is  likely  that  many  patients  classed  as  hysteric 
and  neurasthenic  were  really  suffering  from  thyrotoxicosis. 

In  many  instances  patients  have  not  noticed  that  they  had 
a  tremor  before  the  test  Avas  applied  while  in  others  it  is  so 
great  as  to  constitute  the  chief  complaint. 

It  is  noted  that  the  trembling  of  anger  and  fear  is  very  sim- 
ilar to  that  in  thyroid  intoxication.  Such  Consideration  suggests 
that  the  tremor  is  closely  related  to  hypertension  or  overstimula- 
tion. I  have  frequently  noted  that  beginners  in  pistol  shooting 
impart  the  tremor  to  the  end  of  the  barrel  which  resembles  in 
rate  the  tremor  of  thyroid  intoxication.  This  tremor  is  due  to 
a  too  tight  grip  on  the  stock  of  the  gun  while  under  the  mental 
strain  of  securing  a  bull's  eye. 

The  sign  is  best  elicited  by  having  the  patient  stretch  out  her 
hand  with  the  fingers  spread  out  to  the  maximum  degree.  It  is 
then  usually  visible  to  the  naked  eye  and  is  palpable  by  the  ex- 
amining finger.    The  direction  is  vertical  in  the  pronated  hand. 

The  lower  extremities,  particularly  the  knees,  often  tremble. 
Other  parts,  notably  the  hand  and  tongue,  are  apt  to  show  the 
tremor.  These  tremors  are  usually  present  only  in  the  severer 
cases.     Occasionally  the  tremor  is  intermittent. 

Muscular  Fatigue. — One  of  the  constant  accompaniments  of 


SYMPTOMATOLOGY  95 

tliyrotoxication  is  a  sense  of  iimseular  weakness.  Tlie  patient 
feels  tired,  particularly  in  the  morning,  and  when  she  attempts 
to  exert  herself  she  discovers  that  she  is  tired — that  is  to  say, 
it  is  impossible  for  her  to  undergo  the  former  physical  exertion 
no  matter  how  she  may  try.  Early  this  seems  to  be  but  a  nerv- 
ous exhaustion  state,  for  a  few  doses  of  bromides  may  restore 
to  a  great  extent  the  former  vigor.  The  weakness  is  usually 
ascribed  to  associated  suprarenal  dysfunction.  In  some  of  the 
deeply  pigmented  cases  one  might  think  of  disturbances  of  the 
adrenal.  The  color  is  more  that  of  an  argyria,  however,  than 
that  of  an  Addison's  disease.  Be  this  as  it  may,  bromides  do 
more  to  counteract  it  than  does  epinephrin.  Later  when  their 
is  emaciation  the  weakness  must  be  due  to  actual  muscle 
changes. 

One  of  the  earliest  and  most  striking  phenomena  of  motor 
weakness,  in  a  small  proportion  of  cases,  is  a  weakness  of  the 
knees.  Quite  unawares  the  knees  give  way,  particularly  in  going 
doAMi  stairs.  Sometimes  this  is  the  symptom  that  causes  the  pa- 
tient to  seek  advise.  I  once  had  a  carpenter  consult  me  because 
he  was  unable  to  go  down  a  ladder.  He  had  a  goiter  and  marked 
tachycardia,  but  these  symptoms  had  not  been  noticed.  This 
weakness  is  sometimes  associated  with  or  preceded  by  cramps 
in  the  calves. 

Usually  in  tliyrotoxication  the  tendon  reflexes  are  exagger- 
ated when  the  disease  is  well  developed.  In  the  beginning  and  in 
milder  cases  they  are  normal.  Late  in  the  disease  the  reflexes 
are  sometimes  lost.  AMien  the  reflexes  are  absent  other  causes 
for  their  absence  should  be  sought. 

The  Heart  in  Thyroid  Disease. — It  is  on  the  proper  inter- 
pretation of  the  mechanical  and  functional  state  of  the  heart 
that  the  surgeon's  accuracy  of  operative  prognosis  depends. 
The  most  obvious  sign  is  naturally  the  rate  of  the  beat,  but  the 
state  of  the  heart  muscle  is  the  more  important.  This  state  is 
in  part  only  expressed  in  the  form  and  size  of  the  heart  and  in 
the  working  capacity  as  determined  by  ordinary  clinical 
means.  The  state  of  the  heart  in  goiter  assumes  the  greater  im- 
portance to  the  surgeon  because  the  examination  of  this  organ 
falls  without  the  pale  of  his  ordinary  clinical  investigations  and 
his  medical  consultant  does  not  grasp  the  full  importance  of  es- 


9G  DISEASES    OF    THE    THYROID   GLAND 

Imiatiiig  tlie  exact  Avorkiiig  capacity  of  the  organ  under  the 
added  toxic  and  mechanical  insult  incident  to  the  operation. 
Hence,  though  he  may  have  the  aid  of  a  competent  internist, 
the  responsibility  of  the  final  judgment  rests  on  the  surgeon. 

Tachycardia. — The  most  constant  single  sign  in  toxic  goiter 
is  the  tachycardia.  Not  uncommonly  the  sense  of  increased 
heart  activity  is  the  factor  that  sends  the  patient  in  quest  of 
medical  advice.  All  other  signs  may  occasionally  be  absent  but 
rapid  heart  is  nearly  always  present.  There  are  marked  excep- 
tions to  this  rule.  I  observed  one  patient  with  the  other  classi- 
cal signs  very  pronounced  whose  pulse  did  not  exceed  eighty. 
After  operation  the  pulse  increased  to  100-120.  Nothing  ap- 
peared to  explain  this  anomaly.  The  rate  is  usually  between 
100  and  150  with  90  and  the  limit  of  accountability,  200  or  more, 
as  the  extreme  limits.  The  pulse  rate  is  a  fair  measure  of  the 
intensity  of  the  symptoms.  The  rate  is  habitually  more  rapid  in 
the  morning  than  later  in  the  day  when  the  patient  is  up  and 
about.  This  point  sometimes  helps  to  distinguish  between  a 
toxic  and  a  myocardial  rapid  heart.  It  is  commonly  increased 
by  nervous  excitement,  but  is  influenced  by  drugs  with  difficulty. 
In  some  cases  there  are  attacks  of  extremely  rapid  pulse,  often 
without  apparent  provocation.  Pure  tachycardia  is  not  mark- 
edly affected  by  exercise.  If  it  is  increased  by  exercise  there 
is  most  likely  some  cardiac  muscle  degeneration  already  pres- 
ent. Often  the  patient  is  unable  to  lie  on  her  left  side.  This 
points  to  cardiac  dilatation.  Sometimes  the  patient  is  aware 
of  the  rapid  pulse,  but  quite  as  often  the  patient  is  oblivious 
of  any  trouble.  So  long  as  there  is  no  mj'ocardial  degeneration 
the  rate  is  regular.  Sometimes  there  is  a  subjective  sensation 
of  pulsation  in  the  peripheral  vessels.  Throbbing  in  the  ears 
may  be  the  symptom  most  complained  of.  The  large  arteries 
show  a  pulsation  similar  to  pulsation  in  the  water-hammer  pulse 
in  aortic  regurgitation.  The  aorta  and  large  vessels  of  the  neck, 
particularly  the  superior  thyroid,  pulsate  visibly  and  even  pul- 
sation of  the  parenchymatous  organs  is  said  to  occur.  Epigastric 
pulsation  may  be  pronounced  and  may  constitute  the  chief  dis- 
turbing element. 

The  rate  of  the  heart  is  an  indication  of  the  severity  of  the 
disease,  provided  the  heart  muscle  is  intact.    If  there  is  a  de- 


SWMPTO.MATOLOGY  97 

generation  of  the  muscle,  the  heart  may  be  rehitively  slow  and 
yet  the  patient  be  a  poor  operative  risk.  Usually  the  slow  heart 
presents  evidence  of  fibrillation  and  dilatation  or  other  danger 
signals  of  cardiac  decompensation,  as  well  as  edemas  and  dysp- 
nea on  exertion.  If  there  is  in  addition  to  dyspnea  on  exertion 
some  other  sign  of  weak  heart  muscle,  operation  is  prohibited 
no  matter  what  the  rate.  The  Mayos  place  the  safe  operative 
rate  limit  at  130  and  this  is  as  good  a  conclusion  as  one  may  ex- 
press on  paper,  but  applies  only  when  the  heart  muscle  is  in- 
tact. 

'  The  duration  of  the  disease  gives  a  valuable  clue  in  es- 
timating the  resistance  of  the  heart.  Slight  signs  are  of  graver 
signiticance  in  a  disease  of  some  years'  standing  than  in  a  re- 
cent case.  A  decreasing  rate  is  of  more  favorable  import  than 
an  increasing  one.  For  instance,  given  a  mean  rate  of  130  it  is 
safer  to  operate  on  one  whose  rate  was  150  a  month  or  two  ago 
than  one  of  the  same  rate  who  had  a  rate  of  110  a  like  period 
preceding.  A  rate  which  has  remained  constant  for  a  long  time, 
without  signs  of  cardiac  degeneration  is  less  serious  than  one  re- 
cently developing  the  rapid  rate.  Other  factors  also  enter, 
(liven  a  mean  rate  if  the  patient  is  gaining  in  weight  the  prog- 
nosis is  better  than  the  same  rate  in  one  who  is  losing  weight. 
A  labile  nervous  equilibrium  also  increases  the  gravity  in  the 
presence  of  like  heart  states. 

The  sensitiveness  to  adrenalin  is  a  valuable  determinative 
test  of  the  irritability  of  the  heart.  If  much  excitement  is  pro- 
duced by  adrenalin,  the  patient  will  redact  l)adly  to  operation 
even  in  the  absence  of  cardiac  degeneration.  This  is  a  valuable 
point  in  operating  under  local  anesthesia.  If,  for  instance,  one 
has  decided  to  do  a  lobectomy  and  discovers  after  the  injection 
of  the  novocain  epinephrin  that  the  patiently  is  markedly  ex- 
cited by  it,  he  may  conclude  to  change  his  plan  and  do  a  pole 
ligation  instead. 

Blood  Pressure. — The  blood  pressure  varies  much  in  toxic 
goiter,  often  varying  in  relatively  short  intervals  of  time. 
8trickland-(J()odali  (The  Practitioner,  July,  1900)  classifies  the 
pressure  phenomena  into  three  stages;  (a)  a  state  of  hyper- 
tension, appearing  in  the  primary  stages  and  is  probably  the 
result  of  the  exciting  stimulus  on  the  suprarenal  capsule;  (b) 


98  DISEASES    OF    THE    THYROID   GLAND 

stage  of  hypotension.  At  this  stage  it  is  10  to  20  per  cent  be- 
low the  physiologic  normal  and  is  due  to  peripheral  dilatation. 
This  state  is  due  to  the  action  of  a  depresser  substance  produced 
by  the  gland;  (c)  stage  of  secondaiy  rise  and  is  dependent  on 
the  reduction  of  the  superactivity  of  the  gland  and  to  secondary 
changes  in  the  cardiovascular  system,  such  as  cardiac  hyper- 
trophy. 

It  may  be  readily  conceded  that  there  is  an  early  primary 
rise  if  the  disease  begins  with  a  previously  normal  circulatory 
system.  However,  in  long  pre-existing  colloid  goiters  to  w^hich 
has  been  added  a  myocarditis,  and  secondary  toxicity  develops, 
there  may  begin  at  once  a  marked  depression  in  the  blood  pres- 
sure. This  is  most  tj^pically  noted  in  women  past  the  menopause 
who  have  developed  a  "goiter  heart"  along  with  adiposity  and 
high  blood  pressure.  The  stage  of  hypertension  may  come  early. 
In  the  hyperacute  cases  the  stage  of  preliminary  rise  must  be 
very  short.  I  have  noted  a  depression  within  a  few  weeks  after 
the  onset  of  the  disease.  The  lessened  peripheral  resistance  no 
doubt  has  something  to  do  with  the  fall  but  usually  there  is 
also  a  cardiac  dilatation  or  at  least  a  diffuse,  widened  apex  beat 
with  a  sharp  pulmonary  click.  The  final  rise  of  pressure  pre- 
sages a  spontaneously  developing  recovery. 

Strickland-Goodall  recommends  operation  in  the  stage  of  de- 
pressed blood  pressure,  while  Kocher  recommends  operation 
during  the  period  of  high  pressure.  My  experience  has  been  that 
the  state  of  the  pressure  is  of  little  value,  it  is  the  tendency  alone 
which  is  of  value.  A  rising  low  pressure  may  indicate  a  favor- 
able stage  and  a  maintained  high  pressure  may  indicate  a  safe 
time,  but  a  pressure  may  be  high  and  yet  be  falling,  in  which 
event  it  may  represent  a  highly  improper  time  to  operate.  If 
there  is  a  failing  heart,  operation  is  dangerous  irrespective  of 
the  state  of  the  blood  pressure.  A  single  observation  of  the 
blood  pressure  is  without  value  unless  it  be  very  low,  say  be- 
low a  hundred.  Yet  patients  with  a  long  existing  stationary 
goiter  stand  operation  very  well  with  a  pressure  as  low  as  90. 
Dyspnea  on  exertion  is  a  more  valuable  sign  than  blood  pres- 
sure, for  the  ability  of  the  heart  to  stand  an  increased  demand  is 
what  we  need  to  determine.  Here  also,  one  must  individualize. 
A  patient  may  appear  dyspneic  when  she  is  only  excited.    The 


SYMPTOMATOLOGY  99 

emotional  state  preceding  tlie  dyspneic  state  may  he  the  best 
guide.  Dyspnea  from  pressure  is  relatively  unimportant  as 
compared  to  dyspnea  from  cardiac  weakness.  The  two  are  often 
combined.  This  point  is  likely  to  be  overlooked  in  patients  who 
have  long  had  an  ''innocent"  goiter  who  become  toxic  and 
dyspneic.  Pressure  dyspnea. is  usually  increased  by  assuming- 
certain  positions,  while  cardiac  dyspnea  is  increased  by  exer- 
tion. Edemas  often  show  the  dyspnea  to  be  cardiac  when  the 
displaced  and  compressed  trachea  seems  the  obvious  explana- 
tion. Ocular  inspection  of  the  degree  of  tracheal  stenosis  is  an 
interesting  but  misleading  stunt. 

However  favorable  the  cardiac  state  may  be  such  as  a  rising 
pressure  early  in  the  disease  and  a  decreasing  rate,  the  opera- 
tion may  add  so  much  to  the  toxicity  that  the  heart  muscles  may 
bo  overwhelmed  by  the  load.  If  the  metabolic  destruction  is 
great  no  matter  what  the  apparent  rate  of  the  heart,  operation 
is  interdicted. 

Heart  Sounds. — The  heart  sounds  are  usually  loud  and 
sharp.  Often  in  primary  thyroid  intoxication,  they  are  click- 
ing. It  is  the  heart  beat  of  excitation.  Sometimes  the  apex  beat 
both  on  palpation  and  auscultation  is  diffuse  when  percussion 
and  the  x-ray  show^  an  absence  of  any  enlargement.  This  is  due 
to  the  increased  force  of  the  beat.  The  beat  is  often  so  violent 
tiiat  the  whole  chest  heaves.  Not  infrequently  the  beat  may  be 
heard  some  distance  from  the  chest.  This  is  not  uncommonly 
observed  soon  after  the  injection  of  novocain-epinephrin  solu- 
tion. There  are  sometimes  murmurs  particularly  over  the  base 
without  the  presence  of  anemia  or  demonstrable  enlargement. 
They  are  often  ephemeral.  Reynolds  (Lancet,  1890,  i,  1055) 
found  it  in  two-thirds  of  his  cases.  It  is  difficult  to  say  when  one 
should  designate  the  tones  as  sharp  and  when  as  murmurs.  Eeal 
murmurs,  as  one  heard  them  in  valvular  disease,  are  rare.  In 
many  cases,  of  course,  there  are  organic  lesions  which  existed 
before  the  development  of  the  thyroid  trouble.  In  these  there 
are  usually  the  signs  and  symptoms  that  make  a  diagnosis  pos- 
sible. That  there  is  no  organic  lesion  present  can  only  be  de- 
termined with  certainty  by  their  disappearance  as  the  patient 
recovers  from  the  thyroid  disease. 

The  Goiter  Heart.— The  cardiopathies  associated  with  thy- 


100  DISEASES    OF    THE    THVUOID    (iLAXD 

roid  ciilai'^omoiit  liavo  been  nmcli  discussed  under  the  g-eneral 
caption  of  "Goiter  heart".  Under  this  head  nnist  be  considered 
only  organic  lesions  of  the  heart  and  apart  from  the  mere  in- 
crease of  the  rate.  Some  authors  have  clouded  the  discussion 
by  discussing  under  the  title  diseases  characterized  chiefly  by 
rapid  heart  with  minor  thyroid  changes  and  with  inccmj)letely 
developed  clinical  picture.  There  has  been  much  discussion  as 
to  the  genesis  of  the  cardiac  state  as  observed  in  goiter.  For  the 
purposes  of  this  discussion  but  two  factors  need  be  considered; 
the  conditions  due  to  excitation  dependent  on  the  activity  of  the 
tliyroid  gland,  the  thyrotoxic  heart,  and  that  due  to  mechanical 
liindrance  to  respiration  or  the  circulation. 

The  Thyrotoxic  Heart. — Obviously  theie  are  many  cardiop- 
athies in  wliich  there  are  no  meciianical  factors  operative.  These 
must  be  ascribed  to  the  toxic  action  of  the  goiter.  That  such 
toxicity  is  capable  of  influencing  the  heart  is  indicated  by  the 
Jact  that  it  can  be  artiflcially  produced  by  the  exhibition  of 
gland  substance.  It  is  maintained  by  some  that  the  increased 
rate  of  the  heart  beat  may  be  in  part  due  to  pressure  by  the 
goiter  on  the  heart  regulating  nerves.  These  nerves  by  chang- 
ing the  vascularity  of  the  muscle  influence  the  nutritional  state 
of  the  muscle  and  hence  the  Avork  capacity  of  the  heart. 

There  is  no  direct  connection  with  the  degree  or  duration  of 
the  tachycardia  and  the  extent  of  the  heart  muscle  change.  A 
toxic  goiter  may  exist  many  years  and  yet  the  heart  appear  nor- 
mal. Since  there  is  no  relation  between  the  degree  of  compres- 
sion exerted  by  the  goiter  and  the  degree  of  cardiac  disturbance, 
compression,  believed  to  be  active  in  colloid  goiters,  cannot  be 
operative.  Jf  we  assume  that  the  goiter  elaborates  a  toxic 
substance  capable  of  affecting  the  heart  nmscle,  all  known  fac- 
tors are  employed  and  the  explanation  is  simple — though  we  do 
not  know  the  method  of  action. 

An  actual  widening  of  the  heart's  diameter  in  toxic  goiter 
is  due  mostly  to  an  increase  in  the  size  of  the  cavities  which 
may  in  turn  be  due  to  a  Aveakening  of  the  muscle,  as  seen  in 
acute  Graves'  disease  or  to  a  nmscular  degeneration  as  seen  in 
long-existing  goiter.  Commonly  the  enlargement  is  apparent 
only  due  to  the  increased  violence  of  the  beat. 

Mechanical  Goiter  Heart.— Host   was   the   first   to   ascribe 


SYMPTO-MATOLOCJY  lUl 

the  goiter  lieart  to  tlie  ineeliaiiical  liindraiice  to  respiration.  He 
explained  tliat  the  forced  inspiration  increased  the  negative 
pressure  Avhicli  results  in  an  overfilling  of  the  right  ventricle; 
the  increased  expiratory  effort  tended  to  increase  the  diameter 
of  the  air  passages  with  increase  in  the  interstitial  connective 
tissue  with  subsequent  disturbance  of  the  circulation.  This  is 
plausible  but  incapable  of  proof. 

That  the  patient  may  suffer  nmcli  from  tracheal  stenosis  is 
obvious.  Often  the  patients  do  not  realize  how  much  they  do 
suffer  until  relieved  of  their  obstruction,  and  no  doubt  the  sur- 
geon often  fails  to  appreciate  the  degree  of  their  sutfering.  The 
disturbances  due  to  tracheal  compression  are  in  direct  degree 
to  the  tracheal  compression.  No  doubt  such  stenosis  tends  to 
cause  empliysenia.  Tlie  goiter  hearts  are  by  no  means  confined 
to  those  cases  where  there  is  pronounced  tracheal  compression. 
On  the  contrary,  they  are  as  often  seen  in  those  prominent  goi- 
ters in  which  the  local  disturbance  is  wholly  cosmetic.  That 
mere  compi-ession  does  not  produce  a  goiter  heart  is  indicated 
by  the  fact  that  mediastinal  obstruction  from  other  tumors  may 
exist  for  many  years  without  producing  any  lesion  comparable 
to  goiter  heart.  AVe  may  assume,  therefore,  that  the  simple  col- 
loid goiter  may  elaborate  a  substance  inimical  to  the  normal 
functioning  of  the  heart  muscle. 

Many  complicating  factors  may  enter.  This  type  is  ob- 
served only  in  goiters  capable  of  causing  compression.  These 
patients  are  often  beyond  the  midperiod  of  life.  Often  they 
have  developed  some  cardiac  lesion  independent  of  goiter. 
AVlien  the  long  existent  goiter  becomes  toxic  the  already  diseased 
heart  acts  badly  to  the  stimulus  of  the  goiter.  It  acts  badly  just 
as  it  would  to  any  other  acute  disease.  To  ascribe  all  heart  le- 
sions in  goitrous  patients  to  the  influence  of  the  goiter  but  con- 
fuses the  clinical  ])icture.  The  common  picture  is  as  follows:  a 
patient  beyond  the  age  of  fifty  who  has  borne  many  children  and 
in  the  course  of  years  ha«  developed  a  large  colloid  goiter.  She 
has  gained  in  Aveight,  the  blood  pressure  has  ascended  to  around 
200.  She  is  dyspneic  on  exertion.  Suddenly  she  develops  a 
tremor,  she  loses  rapidly  in  Aveight,  she  becomes  weak  and 
dyspneic.  The  heart  becomes  rapid  and  is  widely  dilated.  This 
is  a  mechanical  goitei-  lienrt.    There  is  no  relation  to  the  degree 


102  DISEASES    OF    THE    THYROID   GLAND 

of  compression  of  the  trachea  and  the  likelihood  of  the  develop- 
ment of  such  a  heart.  It  seems  on  the  contrary  to  be  dependent 
on  abnormal  thyroid  secretion  and  the  old  overM^orked  crippled 
heart  just  cannot  stand  the  pace. 

Digestive  Disturbance. — In  a  disease  so  closely  associated 
with  tlie  nutritional  state,  digestive  disturbance  assumes  a 
double  importance.  There  is  no  symptom  which  varies  more  in 
cases  of  like  severity.  Though  expressive  of  the  goitrous  state, 
it  must  be  remembered  that  a  patient  may  suffer  from  diseases 
of  the  gastrointestinal  tract  which  have  no  relation  to  the  goiter. 
Any  existing  digestive  disorder  should,  therefore,  be  considered 
on  its  own  merits  before  it  is  ascribed  to  the  thyroid  disease. 
Hyperacidity  and  ulcer  are  most  commonly  observed. 

The  Appetite. — Loss  of  appetite  to  complete  anorexia  is 
sometimes  noted,  particularly  in  those  severe  cases  in  which  tlie 
climax  has  been  passed  and  improvement  has  begun  or  is  about 
to  begin.  So  long  as  appetite  is  excessive,  disaster  is  not  immi- 
nent even  though  the  patient  is  still  losing  weight.  In  some 
cases  anorexia  and  excessive  appetite  alternate  or  the  patient 
may  feel  excessive  even  painful  hunger,  but  becomes  nauseated 
at  the  sight  of  food.  When  a  patient  admits  of  an  excessive 
appetite  it  is  important  to  inquire  as  to  the  actual  amount  of 
food  eaten,  for  the  amount  consumed  may  be  relatively  small. 
If  such  be  the  case,  frequent  meals  may  be  desirable. 

Diarrhea. — Diarrhea  is  not  infrequently  noted,  particularly 
in  severe  cases.  They  are  usually  painless,  watery,  grayish  or 
yellow  stools  which  repeat  4  to  8  times  in  a  short  period,  then 
cease  for  some  hours  or  even  days  only  to  recur.  In  rarer 
instances  they  may  persist  for  man}'  months  and  may  then  seri- 
ously menace  the  patient.  This  is  particularly  true  of  those 
made  worse  by  psychic  excitement.  A  true  nervous  colitis,  ca- 
pable of  independent  treatment,  may  exist.  These  are  usually 
seen  in  patients  in  whom  extreme  nervousness  antedates  the  de- 
velopment of  the  thyrotoxic  state.  I  have  never  observed  it  in 
the  true  exophthalmic  type. 

Vomiting. — ^Vomiting  is  a  more  serious  complication.  In 
many  of  the  fatal  cases  persistent  vomiting  is  the  signal  of  ap- 
proaching dissolution.  The  vomitus  is  usually  clear  fluid  but 
may  be  mucus  and  in  extreme  cases  may  be  bloody.    It  occurs 


SYMPTO:^EATOLOGY  103 

irrespective  of  ingestion  of  food,  and  is  most  apt  to  occur  in  the 
morning,  but  may  continue  throughout  the  day.  Sometimes  re- 
curring morning  vomiting  is  followed  by  excessive  appetite  dur- 
ing the  rest  of  the  day.  Most  of  my  cases  of  vomiting  with  an- 
orexia died  within  a  few  days,  while  those  with  intermittent 
\'omiting  recovered.  The  vomiting  is  evidently  central  and  toxic 
because  it  is  not  attended  by  nausea  and  during  the  remissions, 
when  such  occur,  the  digestion  may  not  be  impaired.  A  com- 
l)ination  of  vomiting  and  purging  seems  to  be  very  rare.  Both 
seem  to  be  due  to  a  hyperperistalsis.  There  may  be  persistent 
nausea  without  vomiting.  Miesoicz  (Wien.  klin.  AVchnschr., 
1904,  xvii,  1205)  examined  the  stomach  contents  in  such  cases 
<nid  found  the  secretion  to  be  neutral. 

Constipation. — This  condition  is  often  associated  with 
Graves'  disease.  Sometimes  it  is  particularly  obstinate  before 
the  beginning  of  the  disease.  This  observation  has  led  some  au- 
thors to  assume  an  etiologic  relationship  between  the  constipa- 
tion and  the  goiter.  More  likely  the  constipation  so  noted  is  an 
early  sign  of  the  disease,  since  atony  of  other  muscles  is  often 
noted  as  the  initial  sign.  Xaturally  the  joresence  of  constipation 
may  be  but  the  continuation  of  the  patient's  previous  habits. 
This  is  the  explanation  in  the  majority  of  cases.  In  rare  in- 
stances there  may  be  ol)stinate  constipation  with  vomiting  simu- 
lating an  intestinal  obstruction.  Such  crises  may  precede  the 
recognition  of  the  goitrous  manifestations. 

Icterus. — Icterus  is  a  rare  but  very  significant  symptom. 
In  some  cases  it  is  a  j^art  of  the  terminal  symptom-complex 
particularly  when  associated  with  vomiting.  Even  in  cases  in 
which  it  occurs  early  or  even  j)i'et'(^des  definite  thyrotoxic 
spnptoms,  it  is  indicative  of  severe  affections.  I  operated  on 
one  such  patient  who  seemed  otherwise  a  good  risk,  with  fatal 
results.  All  writers  are  agreed  that  the  icterus  is  a  degenerative 
and  not  a  retention  icterus.  In  such  cases  the  autopsy  shows 
definite  anatomic  changes.  Egier  (Deutsch.  med.  AVchnschr., 
1880,  vi,  3  53)  saw  one  in  which  tliere  was  marked  atrophy  of 
the  right  lol)e  of  the  liver  and  marked  fatty  degeneration.  How- 
ever, Ilaberchron  (Lancet,  1874,  i,  510)  reported  one  autopsy  in 
which  tlie  icterus  seemed  to  be  due  to  a  swelling  of  the  common 
duct.     Even  in  cases  in  which  there  appears  to  be  a  primary 


104  DISEASES    OF    THE    THVR(Ml)    GLAND 

anemia  tlie  liver  has  been  found  atrophic.  Of  eonrse  other 
causes  of  icterus  may  ))e  present.  Eder  (Lancet,  i,  1765)  saw 
icterus  disappear  after  the  patient  jjassed  gallstones.  As  might 
be  expected  gallstones  and  toxic  goiter  may  be  coincident, 
though  tliey  rarely  are  so  associated. 

Intestinal  Hemorrhages. — Bloody  stools  are  sometimes 
noted.  These  are  believed  to  be  associated  with  vasoneuroses. 
[Possible  independent  sources  of  hemorrhage  should  always  be 
sought  ])efore  such  an  exyjlanation  is  accepted,  however.  Me- 
trorrhagia is  sometimes  noted  and  l)leeding  from  the  nose  is 
connnon.  I  saw  one  patient  in  whom  there  was  a  vicarious 
hemorrhage  from  the  nose  during  the  period  of  existing  amen- 
orrhea. Pagoff  (Neurologisches  Centralbl.,  1899,  xviii,  1068) 
saw  hemorrhage  from  the  l)owels  with  metrorrhagia  and  bleed- 
ing from  the  gums.  Intestinal  hemorrhages,  therefore,  likely  are 
an  expression  of  general  vessel  changes  and  not  of  local  disease. 
In  such  cases  there  is  most  likely  a  polyglandular  disturbance 
and  not  truly  a  thyrotoxic  manifestation. 

Changes  in  the  Skin. — In  myxedema  the  skin  is  nmch  thick- 
ened and  the  subcutaneous  tissue  much  increased  so  that  the 
natural  contour  of  the  body  is  lost.  When  the  skin  is  picked  up 
in  folds  the  skin  is  felt  to  be  thick  and  inelastic.  The  increase 
seems  to  be  myxomatous  rather  than  edematous. 

As  one  might  expect  from  the  excited  circulation  in  toxic 
goiter,  the  patient  is  often  suliject  to  sensations  of  heat  and  to 
excessive  perspiration.  These  attacks  sometimes  simulate  like 
sensations  incident  to  the  menopause.  The  hands  and  feet  often 
are  alone  affected  and  in  such  cases  unpleasant  odors  are  en- 
countered. These  symptoms  are  sometimes  most  pronounced  at 
night.  Usually  they  are  but  incidental  to  the  general  course  of 
the  disease,  but  sometimes  they  l)ring  the  jiatient  to  the  physi- 
cian before  the  undei-lying  cause  has  been  diagnosticated. 

Localized,  more  permanent  erythemas  have  been  observed. 
They  not  infrequently  precede  the  not  uncommon  vitiligo  spots. 
The  vitiligo  spots  are  commonly  surrounded  by  deeply  pig- 
mented areas.  Pigmentation  may  be  increased  to  extend  over 
large  areas  and  may  then  suggest  the  pigmentation  of  Addison's 
disease.  That  the  pigmentation  is  directly  associated  with  the 
tliyroid  disturl)ance  is  evidenced  by  the  fact  that  when  the  pri- 


SYMPTOMATOLOGY  105 

iiiary  disease  iini)roves  the  abnormal  ])i^iiieiitation  disappears. 
That  tlie  distiirhaiice  is  not  dependent  on  the  hypersecretion 
is  evident  from  tlie  I'aet  that  pigment  disturbances  attend  myx- 
edema. 

Under  excitement  thyrotoxic  patients  may  flush,  sometimes 
in  localized  areas  and  not  infrequently  show  themselves  subject 
to  urticaria.  Urticarial  lesions  may  be  produced  by  mechanical 
irritation  and  according  to  Peyrou  and  Nair  irritation  from  an 
electrical  current  may  act  in  the  same  way. 

There  does  not  seem  to  be  any  sharp  line  of  demarcation  be- 
tween these  urticarial  lesions  and  more  enduring  edemas.  These 
are  most  connnonly  seen  about  the  eyelids  and  the  extremities. 
These  may  simulate  the  edema  of  myxedema.  Scleroderma  and 
Ilaynaud's  disease  have  been  reported.  The  former  may  be  as- 
sociated with  the  localized  edemas.  Abdominal  dropsies  I  have 
noted  in  a  number  of  instances  in  hyperthyroidism  as  well  as  in 
myxedema.  In  rare  instances  the  hair  l)ecomes  nuich  thinned. 
This  is  more  likely  to  occur  in  myxedema  than  in  hyperthyroid- 
ism. When  there  are  changes  in  the  hair  in  thyrotoxic  cases  a 
transition  to  a  hypofunction  should  be  suspected  and  the 
surgeon  should  guard  his  operative  procedures  with  this  possi- 
bility in  mind. 

Blood  Changes. — Basedow  in  his  original  paper  noted  the 
resemblance  of  goiter  patients  to  the  chlorotics.  Bigelow  (Bos- 
ton Med.  and  Surg.  Jour.,  1859-60,  Ixi,  37)  noted  "pale,  anemic 
girls  with  goiter  and  staring  eyes."  More  recently  the  white 
cells  have  been  studied  closely  which  has  resulted  in  determina- 
tions of  some  practical  value. 

Anemia. — As  above  noted  the  suspicion  was  early  expressed 
that  there  were  blood  changes  in  toxic  goiter.  More  recently 
Roth  (Deutsch.  med.  Wchnschr,  1910,  xxxvi,  259)  has  studied 
this  subject  and  found  moderate  degrees  of  chlorotic  changes  in 
some  instances.  On  the  other  hand,  cases  have  been  reported 
as  chlorotics  in  which  thei'e  was  thyroid  enlargement  and  prom- 
inent eyes.  Innnermann  in  fact  thought  there  was  a  close  rela- 
tionship. 

The  observations  in  this  hospital  seem  to  show  that  there 
is  no  relation  between  toxic  goiter  and  the  hemoglobin  and  red 
cells  of  the  l)lood.     There  is  generally  a  slight  reduction,  the 


106  DISEASES    OF    THE    THYROID   GLAND 

hemoglobin  averages  between  75  and  80  per  cent,  the  red  count 
between  three  and  a  half  and  four  million.  These  are  about 
the  findings  one  would  expect  in  persons  somewhat  under  par  in 
general  health.  If  anemia  exists,  diligent  search  should  be  made 
for  some  complication,  for  be  it  remembered,  the  existence  of 
goiter  does  not  insure  the  patient  freedom  from  other  diseases. 
The  common  causes  for  anemia  are  gynecologic  complications, 
next  gastrointestinal  affections  presenting  the  symptoms  of  ul- 
cer and  mucous  colitis,  and  finally  tuberculosis.  Cases  have  been 
reported  in  which  crises  of  pernicious  anemia  have  antedated  the 
goiter  (DeCostello)  and  of  splenic  anemia  (Variot  and  Ray). 
In  pronounced  secondary  degeneration  in  long  existing  goiter  in 
old  women  there  is  often  a  more  pronounced  general  anemia. 
On  the  contrary,  in  some  of  the  acute  cases  with  hyperemia  or 
in  the  time  of  remission  when  the  gain  in  weight  is  rapid,  the 
red  count  may  go  as  high  as  six  or  seven  million  and  the  hemo- 
globin to  110. 

Generally  speaking,  when  a  patient  with  anemia  is  encoun- 
tered, the  cause  of  the  anemia  should  be  determined  before  she 
is  accepted  as  a  surgical  risk,  not  so  much  because  the  goiter 
operation  will  be  made  more  hazardous,  but  because  the  cause 
of  the  anemia  Avill  not  be  relieved  by  the  cure  of  the  goiter. 

Leucocytosis. — It  was  Kocher's  studies  that  brought  the 
relation  of  the  leucocyte  to  goiter  to  the  front.  He  believed  that 
in  the  relative  increase  in  the  hnnphocytes  was  to  be  found  a 
valuable  diagnostic  and  prognostic  aid.  Unfortunately,  w^hile 
true  in  the  abstract,  for  use  in  the  consideration  of  a  concrete 
case  the  exceptions  are  too  many  to  permit  the  use  of  this 
change.  Generally  speaking  there  is  a  general  leucopenia  of  from 
3,500  to  6,000  but  the  reduction  is  at  the  expense  of  the  poly- 
nuclear  leucocytes,  though  there  may  be  also  an  actual  increase 
of  the  lymphocj^tes.  It  is  knoA\Ti  that  there  is  a  decrease  of  leu- 
cocytes in  starvation  and  the  leucopenia  in  goiters  is  most 
marked  where  loss  of  weight  is  most  pronounced.  Perhaps  the 
dependence  of  the  leucopenia  on  the  toxic  goiter  is  indirect  only. 
Be  this  as  it  may,  in  our  experience  these  changes  do  appear 
in  a  considerable  proportion  of  cases.  Generally  speaking  the 
lymphocytes  amount  to  25  to  45  per  cent  but  may  reach  50  per 
cent  or  beyond.    Sometimes  the  lesser  percentage  of  the  lympho- 


SYMPTOMATOLOGY  107 

cytes  is  compensated  for  by  an  increase  in  the  large  mononu- 
clears, leaving  the  polynuclears  low  in  percentage.  The  varia- 
tions, however,  are  frequent  and  important.  In  some  cases  there 
is  an  actual  leucocytosis  of  moderate  degree.  In  many  of  the 
severer  cases  the  lymphocytes  are  actually  reduced.  In  one  of 
our  severest  cases  they  were  but  6  per  cent.  Various  writers 
liave  sought  to  iron  out  the  discrepancies.  Bracherdt  found  in 
the  transitional  cells  a  balancing  factor,  while  Caro  found  by 
taking  altogether  all  the  mononuclear  forms  the  results  were 
more  constant.  This  seems  to  me  an  important  obsers'ation,  for 
no  doubt  when  the  lymphocytes  are  fewer  than  one  Avould  ex- 
pect the  large  mononuclears  may  show  an  increase.  Kocher  be- 
lieved that  the  lymphocyte  count  gave  a  valuable  prognostic 
help  in  that  within  a  few  days  following  operation  the  relative 
proportionate  count  approaches  normal.  It  is  in  fact  a  common 
observation  that  the  lymphocytes  become  reduced  in  percentage 
on  the  second  or  third  day.  This  does  not  help  us  in  a  practical 
way,  for  if  the  patient  survives  the  operation  so  long,  Ave  may 
be  confident  of  her  recovery.  The  changes  in  the  leucocytes  are 
interesting  but  not  important.  The  decrease  in  the  proportion 
of  the  lymphocytes  is  due  more  to  the  increase  in  the  polynu- 
clears than  in  the  decrease  of  the  lymphocj^tes.  It  has  been 
argued  that  this  increase  of  the  polynuclears  is  due  to  a  reaction 
of  the  operation  per  se  and  not  to  the  fact  that  the  thyroid  has 
been  operated  on.  If  this  were  true,  this  should  subside  when 
the  reaction  has  ceased,  but  this  is  not  true.  There  is  a  perma- 
nent readjustment  toward  the  normal.  The  presence  of  the  toxic 
substance  of  the  thyroid  must  therefore  play  the  determining 
role. 

Kocher  believed  the  determining  cause  of  the  increase  of 
the  lymphocytes  was  the  toxic  substance  in  the  blood  stimulating 
the  spleen  to  give  up  its  leucocytes.  Others,  notably  Klose  and 
Schumacher,  and  Roth  believed  the  interaction  on  the  thymus 
played  a  determining  part.  That  the  thyrotoxic  elements  are 
not  the  determining  factor  is  shown  by  the  fact  that  the  same 
blood  picture  is  found  in  endemic  goiter  and  even  in  myxedema. 
It  should  be  emphasized,  however,  that  the  findings  are  much 
less  constant  in  these  diseases  than  in  the  toxic  type.  One  should 
be  slow  in  concluding  that  colloid  goiter  is  exerting  no  toxic  in- 


108  DISEASES    OF    THE    THYROID   GLAND 

fliieiice  and  tliat  a  myxedema  is  not  a  mixed  affair.  The  hope 
that  the  leucocyte  count  would  give  some  help  in  determination 
of  an  existing  status  thymolymphaticus  has  been  shattered  by 
the  study  of  Kohler.  He  showed  that  the  same  blood  pictures 
are  found  in  a  variety  of  diseases,  noteworthy,  pseudoleukemia, 
Mikulicz's  disease,  diabetes,  nuimps,  hysteria  and  neurasthenia, 
psychoses,  and  during  the  menstrual  period.  It  may  also  be 
remarked  that  it  is  the  normal  state  in  children  and  is  found  not 
infrequently  in  perfectly  healthy  adults. 

If  one  sums  up  the  available  evidence  obtainable  from  a 
study  of  the  leucocytes,  one  is  forced  to  the  conclusion  that  there 
is  some  factor  active  in  toxic  goiter  which  produces  certain 
changes  in  the  leucocytes  but  at  the  present  time  they  are  not 
yet  sufficiently  determined  to  aid  the  clinician  in  a  diagnostic  or 
prognostic  Avay.  The  findings  to  date  are  so  suggestive  that  a 
fui'thor  study  is  nmch  to  be  desired. 

Changes  in  Coagulation  Time. — Lidsky  believes  the  length- 
ening of  the  coagulation  time  is  of  diagnostic  moment  since  he 
found  this  change  in  29  out  of  39  cases  studied,  but  in  a  few 
cases  the  time  Avas  shortened.  Kottmann  likewise  found  it  short- 
ened. In  this  connection  it  should  be  remembered  that  Kuster 
found  the  coagulation  time  in  women  shorter  than  in  men.  An 
attempt  to  use  this  finding  as  a  differential  sign  has  further  been 
upset  l)y  the  fact  that  the  same  findings  were  demonstrated  in 
myxedema.  The  viscosity  of  the  blood  likewise  is  inconstant. 
Kaes  found  it  normal  in  19  per  cent,  reduced  in  50  per  cent  and 
increased  in  31  per  cent. 

The  Adrenalin  Test. — The  increased  sensitiveness  of  thyro- 
toxic patients  to  adrenalin  has  been  known  for  some  time.  Can- 
non observed  that  after  stimulation  of  the  sympathetic,  animals 
were  more  sensitive  to  adrenalin.  Levy  (Am.  Jour.  Physiol., 
1916,  xli,  492)  after  stinndating  the  cervical  sympathetic,  found 
the  animals  more  susceptil)le  to  the  stimulation  of  adrenalin  as 
measured  in  terms  of  blood  pressure.  Since  such  stinmlation 
is  known  to  increase  the  thyroid  secretion,  this  agent  was  be- 
lieved to  be  the  intennediary  factor.  Barker  and  Sladen  (Tr. 
Assn.  Am.  Physicians,  1912,  xxvii,  471)  applied  this  principle 
to  patients  with  goiter  and  discovered  a  considerable  degree  of 
Jiypersensitiveness  to  adrenalin. 


SY:\rPTOMATOLOGY  109 

Tlie  credit  of  developing'  this  test  in  its  workal)le  form  is 
due  to  Goetseh  (New  York  State  Jour.  ;Med.,  1918,  xviii,  259). 
He  used  7.5  minims  (0.5  e.c.)  of  a  1:1000  of  adrenalin  hypoder- 
mically  and  noted  the  effect  on  the  blood  pressure  and  the  gen- 
eral reaction.  In  positive  cases  there  is  a  rise  in  blood  pres- 
sure of  from  10  to  50  mm.  The  noniial  state  is  again  reached 
in  IY2  hours.  The  general  symptoms  of  the  thyrotoxic  state 
are  augmented  at  the  same  time.  A  nuich  smaller  dose  (1 
minim  of  1 :4000)  injected  endennically  produces  a  blanched 
area  at  the  site  of  injection  with  a  peripheral  zone  of  reddening. 
This  lasts  in  the  thyrotoxic  patient  from  li^  to  2^4  hours  Avhile 
in  the  normal  individual  it  disappears  in  30  to  40  minutes. 

The  entlermic  test  just  mentioned  I  have  found  inconstant 
or  at  least  it  is  present  in  nervous  asthenic  individuals  who  pre- 
sent no  other  reason  for  suspecting  hypersecretion.  It  is  pos- 
sible that  many  neuroses  may  ultimately  be  proved  to  be  thyro- 
toxic and  this  test  is  more  valuable  than  we  now  suspect. 

The  hypodermic  injection  of  the  larger  amount  does,  110 
doubt,  augment  the  usual  symptoms  of  thyrotoxicosis.  One 
sees'  this  regularly  in  operation  with  local  anesthetics  containing 
adrenalin.  It  should  not  be  used  as  a  diagnostic  test  in  patients 
in  whom  the  diagnosis  is  evident  because  the  increase  of  the 
symptoms  excites  the  patient  and  makes  her  unduly  apprehen- 
sive of  subsequent  manipulations  and  in  a  few  the  symj)toms 
seem  permanently  increased.  In  slightly  toxic  or  doubtful  cases 
it  may  be  of  use  as  a  means  of  differential  diagnosis,  particu- 
larly in  those  in  whom  there  is  no  apparent  thyroid  enlargement. 

The  chief  value  of  the  knoAvledge  of  this  test  is  in  the  course 
of  operations.  If  the  patient  is  found  to  be  excessiveh'  sensi- 
tive to  the  adrenalin  in  the  local  anesthetic  the  surgeon  had  best 
do  as  little  in  the  way  of  operation  as  jjossible.  Experience  will 
teach  him  the  relation  of  the  reaction  to  operative  resistance. 

Value  of  the  Goetseh  Test. — The  Goetseh  test  may  add  a  link 
to  the  chain  of  evidence.  Standing  alone  it  is  a  curious  phenome- 
non. It  can  be  at  most  but  relative  and  relative  signs  can  never 
stand  alone.  Mariy  persons  not  thyrotoxic  are  susceptil)le  to  ad- 
lenalin;  some  toxic  goiters  are  not.  When  tlie  diagnosis  is  evi- 
dent as  it  nearly  always  is  when  operation  is  in  question,  it 
should  not  be  used.    Its  use  may  frighten  the  patient  to  the  ex- 


110  DISEASES    OF    THE    THYROID   GLAXD 

tent  that  slie  Avill  not  return  to  the  surgeon.  This  is  always  un- 
fortunate for  the  surgeon  and  may  be  bad  for  the  patient. 

As  an  aid  in  determining  the  indication  for  an  operation 
or  as  a  guide  in  judging  its  safety,  it  is  fallacious  and  as  an  aid 
in  determining  the  existence  of  thyrotoxicosis  it  must  be  judi- 
ciously considered  along  with  all  the  other  signs  and  symptoms. 
In  the  consideration  of  toxic  goiters  there  are  always  two  fac- 
tors, the  disease  and  the  patient  and  in  the  use  of  adrenalin  it  is 
not  always  easy  to  determine  whether  the  disease  is  reacting  or 
the  patient.  The  surgeon's  powders  are  limited  to  the  attacking 
of  the  disease  and  the  management  of  the  patient. 

The  chief  value  of  the  test  lies  in  the  fact  that  it  may  give 
one  the  first  clue  in  patients  who  appear  to  be  simply  nervous. 
Sometimes  positive  evidence  of  goiter  does  not  appear  until 
some  years  after  this  test  appears  positive.  In  borderline  cases 
it  can  be  used  to  advantage. 

Basal  Metabolism. — Much  labor  has  been  expended  in  re- 
cent years  in  perfecting  apparatus  for  the  determination  of  the 
metabolic  rate  in  toxic  goiters  and  in  the  determination  of  the 
relation  of  this  to  the  clinical  course  and  operative  risk.  Among 
these  workers  may  be  mentioned  Means  and  Aub  (Jour.  Am. 
Med.  Assn.,  1917,  Ixix,  33);  Boothby  (Boston  Med.  &  Surg. 
Jour.,  1916,  clxxv,  564);  Boothby  and  Sandiford  (Saunders  Co., 
1920)  and  many  others.  By  means  of  gas  apparatus  it  is  sought 
to  determine  the  rate  of  the  bodily  tissue  change,  and  by  this 
means  determine  the  severity  of  the  disease.  In  general  it  may 
be  said  that  there  is  a  direct  relation  demonstrable  in  many 
cases.  Unfortunately  there  are  many  secondary  factors  which 
enter,  such  as  damage  done  to  other  organs,  notably  the  heart. 

Taking  it  as  a  whole,  the  test  becomes  at  once  a  relative 
one,  say  for  instance  like  the  Wassermann  reaction.  It  is  of  value 
if  taken  as  an  adjunct  to  a  careful  clinical  examination  and  if 
done  by  thoroughly  competent  hands.  Unfortunatelj^  the  test 
is  a  difficult  one  to  make  properly  and  error  of  technic  too  often 
comes  in  to  confuse  the  results. 

In  severely  toxic  cases  the  patients  are  often  too  nervous 
to  submit  to  the  restraint  necessary  to  the  test.  An  attempt  to 
apply  the  mask  in  such  cases  may  be  attended  by  permanent 


SYMPTOMATOLOGY  111 

damage  to  the  patient.  This  is  unfortunate,  for  it  is  in  just  this 
class  of  patients  that  the  surgeon  is  most  urgently  in  need  of 
aid. 

On  the  whole,  it  appears  to  be  of  value  in  inverse  ratio  to 
the  clinical  experience  of  the  surgeon.  A  good  laboratory  man 
may  be  of  much  help  to  the  inexperienced  clinician  but  to  the 
experienced  surgeon  the  aid  is  relatively  little  and  a  poor 
laboratory  man  is  a  nuisance  to  both. 

To  make  the  test  the  sole  tribunal  in  the  question  of  the 
presence  or  absence  of  thyrotoxicosis  is  unquestionably  wholly 
wrong.  I  have  seen  a  number  of  discharged  soldiers  with  the 
diagnosis  of  irritable  heart  or  some  such  diagnosis  when  the 
patient  was  typical  Basedow,  eyes  hanging  on  their  faces,  eye 
signs,  tremor,  tachycardia,  goiter,  and  whose  goiter  after  oper- 
ation showed  the  typical  histologic  changes.  Because  there  was 
no  notable  increase  in  metabolic  rate,  thyrotoxicosis  was  de- 
clared to  be  absent. 

It  is  my  judgment  that  the  truth  lies  somewhere  between  the 
views  of  the  skeptic  and  the  enthusiast,  with  the  skeptic  per- 
haps rather  nearer  the  truth.  The  work  along  this  line  should 
be  indulgently  encouraged,  but  critically  analyzed  and  the  re- 
sults accepted  only  when  they  harmonize  with  the  general  clini- 
cal findings. 


CHAPTER  IV 

l)IA(iN()SIS  OF  THYROII)  DISEASE 

111  considering  tlie  diagnosis  of  goiter,  it  must  always  be 
regarded  as  a  constitutional  disease.  Even  in  the  endemic  col- 
loid goiter,  though  it  is  essentially  a  local  process,  no  doubt  the 
general  economy  suffers.  The  thyroid  is  a  guardian  of  the  body, 
and  though  the  effect  of  disturbance  of  it  on  the  general  system 
may  not  be  apparent  in  many  cases,  a  broad  view  must  convince 
one  that  the  influence  is  always  jjresent.  In  the  toxic  forms  the 
systemic  effect  is  apparent.  In  no  case  of  thyroid  disease  should 
a  careful  general  examination  be  omitted.  A  good  diagnosis 
does  not  consist  in  placing  the  patient  in  one  or  the  other  of  the 
groups  of  any  classification  of  thyroid  diseases,  but  the  ability 
to  comprehend  the  deviation  from  the  normal,  not  only  of  the 
thyroid,  but  also  of  every  function  of  the  body.  This  viewpoint 
is  particularly  important  for  the  surgeon  because  from  the  na- 
ture of  his  work,  lie  is  apt  to  concentrate  his  attention  on  a 
lesion  he  can  attack  in  an  operative  way. 

Each  general  group  will  be  considered  in  turn  ever  mindful, 
however,  that  in  many,  no  one  group  will  satisfy  all  the  symp- 
toms the  patient  presents.  Furthermore,  there  is  often  a  fringe 
of  symptoms  that  refuses  to  be  placed  anywhere  in  any  scheme 
of  classification. 

Colloid  Goiter 

Under  this  head  may  be  considered  the  adolescent  goiter, 
which  in  general  signifies  that  the  patient  is  having  some  trou- 
ble in  adjusting  her  endocrine  system  and  the  endemic  colloid 
goiter  which  tends  in  general  to  progress  and  persist.  The  di- 
viding line  is  not  a  sharp  one  but  the  separation  of  the  two  types 
is  helpful  in  deciding  the  treatment. 

Adolescent  Goiter 

Strictly  speaking,  perhaps,  the  adolescent  goiters  are  those 
which  api)oar  only  at  the  developmental  i)eriod  of  life  and  then 

112 


DIAGXOSIS  113 

disappear  again.  However,  often  these  continue  to  develop  and 
assume  a  permanent  place.  These  appear  to  differ  in  no  wise 
from  the  endemic.  In  fact,  it  may  be  open  to  question  whether 
we  can  rightfully  speak  of  any  of  the  goiters  indigenous  to  this 
region  as  "endemic."  At  any  rate,  it  prejudices  nothing  to  re- 
fer to  them  as  simple  colloid  goiters. 

The  adolescent  goiters  are  observed  in  young  persons  be- 
fore the  period  of  maturity  and  are  most  commonly  observed  at 
the  period  of  j)uberty.  The  recognition  of  the  presence  of  an 
enlargement  of  the  thyroid  gland  constitutes  the  diagnosis. 
Fetal  adenomas  appear  as  encapsulated  nodules  in  the  substance 
of  the  gland  and  as  such  form  a  separate  disease. 

Simple  Colloid  Goiters 

In  this  type  there  is  enlargement  of  the  thyroid  gland  con- 
fined to  a  part  or  it  may  involve  more  or  less  the  entire  gland. 
Seldom  in  fact  is  any  part  of  the  gland  wholly  normal.  The 
gland  is  elastic,  freely  movable,  and  not  tender.  When  they 
have  existed  for  a  long  time  they  may  be  dense  because  of  fi- 
brous tissue,  or  hard,  due  to  calcareous  infiltration,  or  soft,  due 
to  cystic  degeneration  of  some  part  of  the  gland.  They  may  be 
lobulated  or  bosselated,  due  to  the  independent  proliferation  of 
some  part  of  the  gland.  The  diagnosis  is  established  by  deter- 
mining that  the  enlargement  represents  the  thyroid  gland,  that 
there  are  no  toxic  symptoms,  and  that  no  secondary  changes 
have  occurred.  If  secondary  changes  have  taken  place,  the 
proper  amendment  to  the  diagnosis  nuist  be  made. 

It  is  usually  easy  to  determine  that  the  tumor  represents  the 
thyroid  gland.  The  tumor  is  attached  to  the  trachea  and  moves 
with  it  in  deglutition.  Dermoids,  cysts  and  lipomas  in  rare  in- 
stances occur  in  the  thyroid  or  are  attached  to  it  and  may  be 
mistaken  for  an  enlargement  of  the  thyroid  gland. 

The  connnoner  forms  of  degeneration  discussed  in  the  sec- 
tion of  pathology,  notably,  the  cystic,  hemorrhagic  and  the  cal- 
careous, are  so  common  as  to  constitute  a  part  of  the  disease. 
The  solitary  cysts  usually  present  isolated,  smooth,  freely  mov- 
able lobules  which  are  very  elastic  or  definitely  fluctuating.  The 
fetal  adenomas  are  equally  encapsulated  but  are  firmer  than  the 
cysts. 


ll-i  DISEASES    OF    THE    THYROID   GLAND 

Secondary  Toxicity 

To  determine  tlie  presence  of  secondary  toxicity  of  a  long- 
existent  goiter,  the  symptoms  detailed  for  primary  toxic  goiter 
are  to  be  songlit.  Usually  the  patient  complains  of  loss  of 
weight  and  increased  nervousness.  The  eye  signs  may  be  pres- 
ent and  tremor  usually  is.  In  many  the  lymphocyte  count  is 
markedly  increased.  If  there  is  progressive  loss  of  Aveight,  the 
metabolism  rate  will  be  increased  and  the  determination  of  it 
is  of  confirmatory  value.  The  Goetsch  test  will  confirm  the 
presence  of  nervousness.  It  is  important  to  remember  that  pa- 
tients Avith  a  colloid  goiter  may  have  complicating  diseases 
which  may  cause  a  loss  of  weight,  and  may  make  them  nervous. 
Therefore  other  cases  should  be  sought  for  these  symptoms. 
An  insipient  tuberculosis  most  often  causes  confusion,  there  is 
usually  a  rise  of  temperature  which  never  occurs  in  toxic  goiters 
mild  enough  to  be  mistaken  for  tuberculosis.  If  the  physi- 
cal signs  of  tuberculosis  are  demonstrable,  the  matter  is  simpli- 
fied. The  two  diseases  may  coexist.  The  presence  of  tubercu- 
losis seems  in  fact  to  have  a  disturbing  influence  on  the  thyroid. 

Malignant  Degeneration 

In  rare  instances  malignant  degeneration  of  an  old  colloid 
goiter  takes  place.  This  is  manifest  (1)  by  a  peculiar  hardness 
which  characterizes  cancer  anywhere;  (2)  by  the  invasion  of 
surrounding  structures;  (3)  by  the  formation  of  metastases  else- 
where in  the  body.  The  hardness  is  seldom  pathognomonic  be- 
cause the  nonmalignant  gland  is  often  hard.  It  is  only  when 
small  nodular  protrusions,  apparently  of  recent  growth,  appear 
that  the  suggestion  becomes  impressive.  Often  the  gland  may 
manifest  malignancy  by  forming  metastases  Avhen  its  consist- 
ency and  the  anatomic  structure  do  not  show  any  decided 
change  from  the  normal,  therefore  clinical  examination  often 
leaves  us  nothing  more  tangible  than  a  suspicion.  The  invasion 
of  the  surrounding  tissue,  when  definite  and  pronounced,  is  im- 
pressive and  certain.  The  nuiscles  are  the  first  to  become  in- 
volved, but  the  esophagus  and  trachea  may  become  iiwaded.  In 
order  that  one  may  make  a  diagnosis  of  invasion,  tumor  nodules 
must  be  felt  beyond  the  confines  of  the  goiter  if  one  is  to  be  cer- 


DIAGNOSIS  115 

tain,  ^[ere  attachment  to  the  snrronnding  tissue  may  be  sim- 
ulated by  a  jjeritliyroiditis.  If  there  is  comj^lete  tixation  of  the 
trachea  without  definite  symptoms  of  inflammatory  reaction, 
malignancy  is  suggested.  Pronounced  enlargement  of  the  skin 
veins,  particularly  if  unilateral,  presents  additional  evidence  in 
favor  of  malignancy.  If  susiDicions  of  local  malignancy  are 
coupled  with  metastasis  elsewhere  the  probability  is  increased. 
If  such  metastasis  shows  thyroid  structure,  the  malignant  char- 
acter of  the  thyroid  is  proved  no  matter  what  the  local  findings 
in  the  thyroid  may  be.  In  a  number  of  instances  of  metastatic 
tumors  in  my  experience  the  thyroid  was  not  suspected,  even 
the  presence  of  a  goiter  was  not  noted,  until  the  supposedly  pri- 
mary tumor  elsewhere  proved  to  be  of  thyroid  origin.  The 
bones  most  frequently  show  such  metastases,  notably  the  hu- 
merus, the  iliac,  and  the  skull  bones  are  most  likely  to  be  in- 
vaded. The  intestinal  tract  has  been  the  seat  in  a  number  of 
instances. 

Affections  of  Other  Organs 

In  colloid  goiters  other  organs,  notably  the  heart  and 
lungs,  may  show  involvement.  The  heart  may  presenc  the 
usual  symptoms  of  fibrillation  and  myocardial  degeneration. 
These  symptoms  likely  are  the  result  of  an  intoxication  froiK 
the  ''innocent"  goiter.  When  the  rapid  pulse  is  associated  with 
nervousness,  the  goiter  may  erroneously  be  regarded  as  toxic. 
Loss  of  weight  and  tremor  may  aid  in  the  differentiation.  In 
many  of  the  secondarily  toxic  goiters  the  lesions  characteristic 
of  myocardial  degeneration  may  coexist  with  the  tachycardia 
of  thyrotoxicosis.  In  such  combined  disturbances  the  relative 
part  each  plays  can  best  be  determined  by  putting  the  patient  in 
bed  and  treating  the  heart  as  a  myocardial  lesion.  As  this  iiii-- 
jjroves,  the  extent  of  the  actual  tachycardia  becomes  more  ap- 
parent. An  irregular  heart  from  primary  myocardial  lesion 
stands  operation  better  than  one  Avhich  has  become  irregular  fol- 
lowing the  toxic  changes  in  the  goiter. 

The  lungs  often  are  involved  in  simple  goiter  because  of 
pressure  on  the  trachea  or  large  vessels  of  the  neck.  This  is 
said  to  lead  to  emphysema,  possibly  to  bronchiectasis  and  par- 
ticularly to  secondary  involvement  of  the  heart,  the  so-called 


116  DISEASES    OF    THE    THYROID   GIAXD 

o-oiter  heart.  It  seems  a  bit  far  fetclied  to  ascTil)e  the  heart  in- 
volvement to  pressure  of  the  goiter  on  the  vessels.  One  sees 
the  heart  involved  when  there  is  no  evidence  of  interference 
with  the  vessels  and  it  may  be  absent  when  there  is  obvious 
pressure  on  the  vessels.  This  leads  me  to  the  opinion  that  the 
'* simple"  goiter  may  poison  the  heart.  This  seems  doubly  so 
because  when  the  heart  is  affected  the  goiter  shows  marked  cel- 
lular and  colloidal  degeneration. 

Toxic  Goiter 

In  harmony  with  the  preceding  remarks  in  the  considera- 
tion of  toxic  goiter  it  is  well  for  the  surgeon  to  consider  w^ell 
whether  he  has  a  goiter  which  developed  along  with  the  gen- 
eral symptoms  of  thyrotoxicosis  or  whether  the  general  symp- 
toms were  implanted  on  a  long  existing  goiter.  In  the  former 
ill  the  beginning  he  likely  has  the  cooperation  of  a  normal  bod- 
ily function  affected  only  by  the  toxic  material  of  the  goiter, 
while  in  the  latter  he  may  have  pre-existing  changes  in  addition 
to  those  produced  by  the  toxic  goiter. 

Primary  toxic  goiters  may  be  separated  into  the  exoph- 
thalmic and  the  nonexophthalmic  type.  In  the  former  the  eye 
signs  form  the  important  chain  in  the  symptomatology.  The 
various  eye  signs  detailed  in  the  chapter  on  symptomatology 
are  pathognomonic  of  toxic  goiter.  The  nonexophthalmic  type 
may  present  like  symptomatology  in  other  respects  and  wiien 
goiter,  tremor  and  tachycardia  are  present,  the  diagnosis  offers 
no  difficulty. 

The  present  tendency  to  exclude  cases  as  not  genuine  if 
there  is  a  lack  of  metabolic  disturbance  that  can  be  shown  by 
the  machine,  is  to  be  deprecated.  There  have  been  examples 
enough  of  the  fallacy  of  allowing  scientific  refinements  to  upset 
clinical  experience  without  adding  this  to  the  list.  If  the  typical 
symptoms  are  present  the  diagnosis  is  made  irrespective  of  the 
metabolic  rate.  Toxic  goiter  is  notoriously  a  disease  of  waves, 
and  if  the  observation  is  made  in  a  quiescent  period  or  when 
the  disease  is  regressive,  the  metabolic  rate  will  not  show  the 
extent  or  even  the  presence  of  the  disease.  The  patient  is  a 
thyrotoxic  one  albeit  one  in  the  stage  of  remission. 

Ill  rarer  instances  the  goiter  may  be  absent.    In  the  pres- 


DIAGNOSIS  117 

ence  of  eye  signs,  taeliycardia  and  tremor  the  diagnosis  is  cer- 
tain. In  the  absence  of  eye  signs  the  problem  is  more  difficult. 
The  tremor,  tachycardia,  and  loss  of  weight  are  suggestive,  but  a 
probable  diagnosis  can  be  arrived  at  only  by  a  careful  considera- 
tion of  the  vai'ious  diseases  that  may  cause  each  of  these  symp- 
toms singly  or  collectively. 

Neuropathic  tachycardia  is  intermittent,  the  periods  of  re- 
mission being  attended  by  a  normal  pulse  rate.  There  is  an  ab- 
sence of  tremor  and  loss  of  weight.  The  tachycardia  may  us- 
ually be  controlled  by  proper  remedial  measures  which  have  no 
influence  on  the  thyrotoxic  tachycardia. 

The  neurogenic  tremors  are  coarser  and  not  so  fast  as  the 
tremor  of  thyrotoxicosis  and  they  are  not  attended  by  a  rapid 
heart  or  loss  of  weight. 

Rapid  heart  and  loss  of  weight  are  often  the  accompani- 
ments of  incipient  tuberculosis.  When  there  is  a  palpable  en- 
largement of  the  thyroid,  the  differentiation  is  often  difficult. 
The  presence  of  rise  of  temperature  is  the  most  valuable  differen- 
tial sign  as  has  already  been  mentioned.  In  toxic  goiters  of  mild 
degree  there  is  no  rise  of  temperature.  One  may  find  physical 
signs  of  tuberculosis,  the  muscle  signs,  loss  of  vesicular  breath 
sounds  or  the  increase  of  them,  particularly  if  rales  can  be  dis- 
covered, the  problem  is  then  simplified.  Cough  is  not  an  early 
sign  of  tuberculosis  and  its  absence  should  not  be  considered  as 
a  negative  sign  of  value.  The  various  tests  are  of  little  value; 
among  these  may  be  considered  the  von  Pirquet  for  tuberculosis 
and  the  Goetsch  for  thyrotoxicosis.  If  relied  upon,  standing 
alone,  they  are  more  apt  to  mislead  than  to  aid.  If  after  care- 
ful physical  examination  there  is  doubt,  the  case  had  best  be 
considered  as  one  of  tuberculosis.  It  will  be  an  error  on  the  side 
of  safety  and  the  guess  will  nearly  always  be  right.  At  any 
rate,  the  proper  treatment  in  each  case  is  rest.  The  surgeon 
can  find  comfort  in  the  fact  that  a  goiter  patient  with  fever  is 
not  a  fit  subject  for  operative  treatment  and  the  knottier  prob- 
lem of  lung  diagnosis  may  be  left  for  the  lung  specialist. 

Secondary  Toxic  Goiter 

The  diagnosis  rarely  offers  great  difficulty.  The  border- 
land cases  have  already  been  discussed.    The  patient  nearly  al- 


118  DISEASES    OF    THE    THYROID   GLAXD 

ways  presents  an  evident  goiter  of  many  years'  duration.  Added 
to  this  are  tlie  toxic  symptoms.  These  consist  of  nervousness 
both  subjective  and  objective.  Eye  signs  are  rarely  present, 
never  in  the  pure  degenerative  forms.  Tremor  is  a  marked 
sign  and  tachycardia  and  loss  of  weight  are  prominent.  The 
thyroid  often  is  hard  and  elastic  and  very  often  is  sensitive  to 
pressure  and  may  show  a  degree  of  fixation.  These  local  signs 
are  of  great  value  in  deciding  the  degree  of  responsibility  that 
should  be  ascribed  to  the  goiter.  Often  there  is  pain  in  the  re- 
gion of  the  mastoid  and  occasionally  dilatation  of  the  corres- 
ponding pupil.  Xot  infrequently  the  local  reaction  on  the  part  of 
the  goiter  may  amount  to  a  veritable  nonsuppurative  thyroid- 
itis. Fever  and  delirium  frequently  are  present.  These  severer 
forms  are  most  commonly  observed  in  women  past  the  meno- 
pause. 

In  the  milder  types  a  careful  general  examination  must  be 
taken  into  account.  This  is  particularly  true  of  those  Avho  are 
in  the  mid-child-bearing  period.  Here  pelvic  lesions,  particu- 
larly those  resulting  from  child-bearing,  must  be  carefully  con- 
sidered. Loss  of  weight  and  nervousness  are  often  pronounced, 
but  the  nervousness  is  usually  subjective  and  the  tachycardia 
if  present  is  ephemeral  and  disappears  on  rest  in  bed.  The  neu- 
rotic may  present  a  tremor  i)articularly  if  the  sign  is  often 
sought  after,  giving  her  the  impression  that  it  will  add  to  the 
general  interest  if  she  has  one,  but  it  is  not  the  tine  tremor  of 
the  thyrotoxic  patient. 

Unfortunately  this  type  of  thyrotoxic  patient  usually  has 
some  genital  lesion  and  it  requires  fine  judgment  to  determine 
how  much  each  disease  adds  to  the  sum  total  of  the  patient's 
complaint.  This  is  necessary  in  order  to  determine  how  much 
improvement  will  follow  the  correction  of  either  evil.  A  vertex 
or  occipital  headache,  a  lumbar  backache  or  a  leucorrhea  will 
not  be  cured  by  the  removal  of  a  part  of  the  thyroid  gland.  The 
dominant  lesion  may  often  best  be  judged  by  noting  the  pa- 
tient's viewpoint.  If  she  voluntarily  offers  at  the  first  meeting 
that  she  is  suffering  from  a  chain  of  symptoms  which  the  sur- 
geon recognizes  as  of  pelvic  origin  this  should  be  regarded  as 
likely  the  dominant  disease,  even  though  she  be  carrying  a 
goiter  that  the  surgeon  covets.    If  the  surgeon  operates  for  the 


DIAGlfOSIS  119 

relief  of  one  ailment  and  the  patient  expects  relief  from,  another, 
misunderstanding  may  arise. 

Atypical  Forms 

In  some  cases  some  of  the  dominant  symptoms  are  lacking. 
In  most  cases,  as  a  matter  of  fact,  the  eye  signs  are  absent.  In 
such  cases,  some  care  may  discover  eye  signs  otherwise  regarded 
as  absent.  One  eye  alone  may  be  affected.  The  eye  signs  may 
be  positive  Avhen  the  patient  is  under  excitement,  as  after  the 
administration  of  adrenalin,  either  during  the  operation  or  in 
the  use  of  the  Goetsch  test.  In  some  the  goiter  is  absent,  in  rare 
instances  the  pulse  rate  is  slow  and  very  rarely  the  tremor  is  ab- 
sent. These  atypical  forms  have  been  erroneously  classified  with 
the  forme  fruste.  In  the  atypical  forms,  the  symptoms  that  are 
present  do  not  vary  in  any  essential  manner  from  the  true  form. 
The  character  of  the  apex  beat  when  tachycardia  is  the  only 
symptom  is  very  suggestive.  If  it  is  more  rapid  in  the  morning 
than  in  the  afternoon  when  the  patient  is  left  quietly  in  bed,  this 
fact  is  in  itself  enough  to  warrant  a  presumptive  diagnosis.  This 
is  particularly  true  of  the  tremor.  It  is  very  fine  and  is  con- 
stantly present.  When  the  tachycardia  and  the  tremor  both  are 
present,  a  diagnosis  may  be  hazarded.  The  heart  may  be  slow 
but  the  heart  outline  may  be  increased,  the  neck  vessels  full  and 
pulsating,  in  fact  all  the  usual  symptoms  of  the  circulatory  dis- 
turbance of  toxic  goiter  except  the  rate.  The  goiter  may  ap- 
pear to  be  absent  while  it  really  is  present  though  substernal  or 
aberrant.  It  may  appear  for  a  short  time  then  recede  without 
there  being  any  notable  change  in  the  symptomatology.  These 
atypical  forms  may  be  very  severe,  even  to  the  development  of 
delirium  and  high  fever.  Because  of  these  symptoms  a  general 
infection  such  as  malignant  endocarditis  may  be  suspected; 

Hyperacute  Forms 

In  rare  instances  toxic  goiters  come  on  with  amazing  sud- 
denness. Nervousness,  delirium  and  fever  and  often  vomiting 
may  set  in  within  the  first  few  days.  They  may  even  have  the 
violent  symptoms  of  an  acute  mania.  If  eye  signs  are  present 
and  tlie  thyroid  is  enlarged,  the  diagnosis  is  fairly  easy.  One 
must  be  careful  in  judging  the  eye  symptoms,  for  febrile,  de- 


120  DISEASES    OF    THE    THYROID   GLAND 

lirioiis  patients  liave  a  staring  look  and  one  is  not  able  to  satis- 
factorily test  out  the  finer  movements  of  the  eyes  and  the  eye- 
lids because  of  the  mental  state.  The  tremor  is  usually  marked 
and  the  neck  vessels  violently  throbbing-.  There  is  rapid 
emaciation  though  this  sign  may  be  of  little  use  because  the 
fever  and  vomiting  may  appear  to  account  for  it.  When  there 
is  no  thyroid  enlargement  one  may  not  suspect  the  possibility  of 
a  toxic  goiter  and  Avill  consider  only  acute  mental  excitation  and 
the  general  symptoms  of  intoxication.  If  the  heart  signs  dom- 
inate or  the  excitation  be  slight,  one  may  suspect  an  inflamma- 
tory cardiac  lesion.  However,  the  tumultuousness  of  the  cardiac 
activity  should  cause  one  to  suspect  the  true  nature  of  the 
trouble.  Usually  there  is  the  characteristic  tremor  which  gives 
one  the  clew.  If  the  sign  is  searched  for  often  one  finds  the 
thyroid  region  sensitive  even  if  the  goiter  is  not  definitely  pal- 
pable. Nearly  always  sooner  or  later  the  thyroid  enlargement 
appears. 

These  cases  usually  run  their  course  in  ten  days  to  three 
weeks  which  is  more  rapid  than  the  diseases  it  simulates  usually 
run  their  course.  Sometimes  one  only  suspects  the  disease  and 
an  extremely  degenerated  state  of  the  thyroid  furnishes  the  final 
point  in  diagnosis. 

Interstitial  Type  (Forme  Fruste) 

By  the  forme  fruste  is  understood  a  type  of  thyroid  disturb- 
ance which  differs  from  the  regular  form  by  the  predominat- 
ingly nervous  symptoms,  usually  of  an  indefinite  nature,  and  by 
its  little  tendency  to  remit  or  recover  or  to  become  progressively 
worse.  This  type  is  to  be  sharply  separated  from  the  atypical 
forms  already  discussed. 

This  type  was  named  Forme  Fruste  by  Charcot  (Gaz.  d. 
Hosp.,  1885,  No.  15)  and  by  (1.  Marie  (Contribution  a  I'stude  et 
an  diagnostic  des  formes  frustes  de  la  Maladie  de  Basedow, 
Paris,  1883)  because  they  believed  it  represented  an  incomplete 
type  of  Graves'  disease.  This  assumption  has  led  to  endless 
embarrassment  to  the  operating  surgeon.  According  to  Charcot 
forme  fruste  represents  a  type  of  the  disease  made  up  of  one 
or  more  of  the  chief  triad  symptoms  (exophthalmos,  goiter, 
tachycardia  and  to  these  he  added  tremor)  with  a  number  of 


DIAGNOSIS  121 

secondary  syinptoins,  such  as  digestive  disturbances,  nervous 
sjanptoins,  disturbances  in  resjiiration,  disturl)ances  in  the  gen- 
ital spliere  and  in  the  urinary  secretion.  In  drawing  the 
analogy  Charcot  was  guided  only  by  symptoms  present  at  a 
given  time.  He  ignored  entirely  the  fact  that  the  onset,  the  in- 
herent physical  substratum  and  the  final  course  were  without 
definite  similarity  to  the  typical  Basedow's  disease.  There  are 
any  number  of  instances  in  medical  history  where  like  error  in 
logic  ended  in  confusion.  Chancre  and  chancroid,  typhus  and 
typhoid  may  be  cited  as  instances. 

Whatever  may  be  the  ultimate  solution  of  the  question  of 
relation,  however,  the  classic  Basedow  and  the  forme  fruste, 
surgical  experience  has  emphatically  proved  that  the  prognosis 
is  wholly  different  and  so  far  as  the  surgeon's  activities  are 
concerned  the  relationship  between  the  two  diseases  is  not  very 
close. 

There  is  a  wide  divergence  of  opinion  among  neurologists 
as  to  the  relation  of  this  disease  to  Graves'  disease  on  the  one 
hand  and  unrelated  neuroses  on  the  other.  To  neurologists  it  is 
largely  an  academic  question,  but  to  surgeons  it  is  more  vital. 
Nevertheless  there  is  a  constancy  in  the  symptomatology  and 
course  which  bespeaks  a  fundamental  pathologic  defect  but  re- 
garding it  we  are  yet  in  the  dark.  Unfortunately  we  cannot  at- 
tack the  problem  as  yet  on  the  only  certain  basis,  that  of 
etiology,  consequently  the  prognosis  is  the  most  reliable  guide. 

The  most  constant  phenomena  found  in  this  class  of  pa- 
tients is  that  they  are  primarily  nervous,  irritable,  sleepless,  of- 
ten showing  definite  neuropathic  manifestations,  as  epilepsy  or 
mental  aberration.  The  disease  begins  in  early  adult  life;  often 
there  are  a  number  of  cases  in  the  same  famil}^,  not  infrequently 
representatives  of  both  sexes.  They  are  usually  long  and  thin 
of  build.  Their  chief  symptom  is  nervousness.  They  are  liy- 
peresthetic  and  often  the  reflexes  are  increased.  They  have  a 
fine  tremor  which  becomes^worse  under  excitement.  They  pre- 
sent small,  fairly  firm,  uniformly  enlarged  smooth  goiters  which 
are  often  sensitive  to  touch.  The  patient  often  complains  of 
choking  sensations,  particularly  if  she  knows  of  the  presence  of 
an  "inward  goiter."  These  often  resemble  the  symptoms  of 
globus   hystericus   and   quite   possibly  they   are   synonymous. 


122  DISEASES   OF   THE   THYROID   GLAND 

These  symptoms  are  wholly  different  from  those  in  which  there 
is  actual  compression  of  the  trachea  by  the  goiter.  When  ac- 
tual tracheal  compression  exists,  so  slow  has  been  its  develop- 
ment that  the  patient  is  inclined  to  minimize  its  extent. 

These  patients  are  apprehensive  of  everything  and  observe 
their  nmltitudinous  symptoms  with  the  minute  care  of  a  sym- 
pathetic scientist.  Often  they  come  armed  with  a  manuscript 
copy  of  their  various  complaints,  apprehensive  that  in  their 
recitation  of  symptoms  some  of  them  might  inadvertently  be 
overlooked. 

They  are  sensitive  to  everything.  They  respond  to  the 
Goetsch  test  and  are  hypersensitive  to  thyroid  extract  and,  ac- 
cording to  Charcot,  they  have  a  lessened  resistance  to  the  elec- 
trical current,  but  they  react  badly  to  nerve  sedatives. 

The  loss  of  weight  varies,  but  usually  amounts  to  10  to  25 
pounds.  Usually  the  normal  weight  exceeds  a  hundred  pounds 
but  slightly,  so  that  the  loss  of  a  few  pounds  is  an  important 
matter  to  them.  The  weight  usually  fluctuates  a  few  pounds  up 
and  down  from  year  to  year. 

Associated  with  these  symptoms  there  is  usually  evidence 
of  ovarian  hypoplasia.  The  menses  usually  begin  late.  The 
patient  has  a  scanty  menstruation;  generally  there  are  cramps 
in  the  beginning  and  the  patient  is  often  obliged  to  take  to  her 
bed  during  the  first  few  hours.  The  genital  organs  are  hypo- 
plastic and  frequently  the  small  uterus  is  displaced  backwards 
or  the  small  flat  cervix  points  in  the  axis  of  the  vagina.  The 
ovaries  are  small,  hard  and  the  surface  puckered  and  contain 
few  or  no  follicles.  Often  these  phenomena  exist  for  years  be- 
fore a  thyroid  enlargement  and  rapid  pulse  manifest  them- 
selves. Forme  fruste  with  normal  pelvic  organs  is  unusual,  to 
say  the  least.  The  belief  that  there  is  a  relationship  to  the 
ovaries  is  strengthened  by  the  fact  that  many  of  the  symptoms 
of  this  disease  are  simulated  in  the  complaints  of  the  castrated. 

One  nuist  differentiate  these  patients  from  those  who  have 
adolescent  goiter  with  neuropathic  symptoms.  However,  the 
menstrual  disturbance  is  not  scant,  not  delayed,  and  the  pain 
if  any,  is  definitely  spasmodic  in  the  adolescent  form.  Moreover 
their  nervousness  is  of  the  vulgar  type  while  the  true  forme 
fruste  has  raised  her  nervousness  to  an  art.    The  course  also  de- 


DIAGNOSIS  123 

fines  the  difterence.  The  adolescent  goiters  recover  with  or  with- 
out treatment  and  often  respond  quicklj^  to  sedative  treatment; 
or  if  not,  when  they  gain  the  rank  of  matrons  their  symptoms 
lessen. 

The  loss  of  weight  accompanied  by  marked  weakness  often 
raises  the  question  of  tuberculosis,  and  if  the  observer  is  in- 
clined to  a  specialty  in  that  disease,  he  is  apt  to  render  this  as 
the  probable  diagnosis.  Seldom  does  the  tuberculous  patient 
show  the  nervous  apprehension  of  the  goiter  patient,  and  the 
tremor  is  not  present  in  tuberculosis.  Tuberculosis  specialists 
have  a  neat  way  of  escaping,  when  later  developments  indicate 
a  positive  diagnosis  of  thyroid  disease,  by  declaring  an  associa- 
tion of  the  two  diseases,  the  tuberculosis  having  healed  as  the 
thyroid  disease  grew  worse. 

The  most  constant  symptom  in  the  forme  fruste  disease  is 
the  rapid  heart.  The  increase  in  rate  does  not  approach  that  of 
the  real  toxic  goiter.  The  rate  is  usually  90  to  110.  The  pulse 
is  small  and  the  neck  vessels  do  not  pulsate.  The  blood  pres- 
sure, instead  of  being  increased  as  in  thyrotoxicosis,  is  dimin- 
ished; usually  it  varies  between  95  and  110.  This  has  led  some 
observers  to  designate  this  disease  as  a  "Basedow  heart."  This 
is  unfortunate  because  a  rapid  heart  is  no  more  a  specific  symp- 
tom in  disease  involving  the  thyroid,  than  is  pain  in  the  differ- 
entiation of  abdominal  diseases.  As  a  matter  of  fact,  the  heart 
other  than  its  rate  is  little  affected.  Dilatation  is  uncommon 
and  murmurs  even  more  so. 

Earely  this  type  develops  into  a  more  pronounced  type  of 
thyroid  intoxication,  having  the  classical  symptoms.  I  recently 
observed  a  patient  who  had  suffered  from  the  milder  type  of  the 
disease  for  many  years,  suddenly  develop  a  pronounced  goiter, 
cardiac  dilation,  and  nervousness.  She  died  spontaneously 
three  months  later.  This  patient  had,  however,  a  large  colloid 
goiter  which  ran  the  course  of  a  secondary  toxic  goiter  after  the 
menopause.  She  had  two  sons  and  a  daughter  victims  of  forme 
fruste.  This  fact  makes  one  somewhat  reserved  in  expressing 
a  prognosis. 

The  chief  difficulty  in  the  diagnosis  of  this  type  is  that 
typically  neurotic  persons  may  develop  any  of  the  common 
types  of  goiter.    As  a  matter  of  fact,  many  neurologists  main- 


124  DISEASES    OF    THE    THYROID   GLAND 

tain  that  all  toxic  goiters  have  a  neuropathic  substratum.  "When 
a  change  in  type  occurs  tlie  heart  rate  may  become  more  rapid 
and  the  apex  become  broader  and  the  neck  vessels  pulsate. 

Evidence  of  metabolic  disturbance  in  these  cases  is  usually 
wanting  and  is  never  pronounced.  The  blood  changes,  notably 
the  lymphocytosis  is  within  a  possible  normal  for  such  individ- 
uals, generally  hypoplastic. 

The  chemistry  of  this  is  the  important  element  in  the  diag- 
nosis. The  more  pronounced  the  symptoms  of  a  goitrous  na- 
ture, the  better  the  prospect  of  improvement.  Usually  after 
years  the  thyroid  enlargement  disappears,  but  the  nervous 
symptoms  continue,  years  without  end.  There  are  many  who 
have  the  symptom-complex  without  goiter  and  in  all  of  them  one 
gets  the  impression  that  the  atfair  is  dominantly  neurotic.  This 
supposition  is  heightened  by  the  fact  that  operation  influences 
the  course  but  little.  The  more  pronounced  the  nervous  el- 
ements, the  less  the  prospect  of  any  improvement.  In  this,  Na- 
ture has  been  kind:  underdeveloped,  they  are  unfit  for  mother- 
hood and  they  dote  on  their  symptoms  with  the  same  care  they 
might  a  brood  of  offspring.  Some  who  bear  children  seem  to  be 
improved  by  it,  the  ovarian  function  seems  in  a  measure  to  gain 
a  balance  of  power.  Quite  as  commonly  the  burdens  of  mother- 
hood add  new  features  of  irritation,  and  pelvic  disease  is  added 
to  the  complex. 


CHAPTER  V 

PROGNOSIS  IN  DISEASE  OF  THE  THYROID 

No  phase  in  tlie  discussion  of  a  disease  is  so  difficult  as  the 
abstract  consideration  of  prognosis.  It  implies  the  use  of  statis- 
tics, yet  the  use  of  statistics  is  doubly  difficult  in  a  disease  like 
that  of  goiter  in  which  the  question  of  cure  cannot  be  definitely 
•determined  ami  the  estimate  of  the  degree  of  improvement  is  al- 
ways colored  b}'  the  personal  equation  of  both  patient  and  sur- 
geon. The  question  of  mortality  after  operation  likewise  cannot 
be  stated  in  general  terms.  The  results  of  the  tyro  and  the  ex- 
j)ei-t,  as  regards  operative  results,  are  more  divergent  than  after 
any  other  surgical  procedure.  The  results  of  one  operator  can- 
not be  used  in  the  slightest  degree  in  estimating  the  probable 
operative  risk  in  the  hands  of  another  operator. 

Even  in  the  study  of  one's  own  results  the  difficulties  are 
many.  I  am  becoming  more  skeptical  as  to  the  prognosis  the 
more  closely  I  study  my  patients.  Like  operating  on  malignant 
disease,  the  operative  recovery  is  only  a  part  of  the  story. 
Nearly  all  patients  operated  on  show  postoperative  improve- 
nient.  In  some  instances  the  patient  thinks  herself  well  and 
w^rites  glowing  accounts  of  her  improved  condition.  Reports  by 
correspondence  are  of  limited  use.  Often  those  that  report  by 
letter  that  they  are  quite  well  will  be  found  on  examination  to 
have  still  some  of  their  old  symptoms.  For  purposes  of  com- 
parison, therefore  it  is  necessary  that  the  clinician,  or  one  who 
employs  the  same  language,  should  check  up  the  results  from 
time  to  time  by  actual  examination  of  the  patient.  When  the  pa- 
tient declares  herself  quite  well  and  the  examiner  finds  evidence 
of  the  former  symptoms, -whose  opinion  shall  prevail  in  the 
formulation  of  statistics! 

Statistical  records  correct  today  may  be  all  wrong  at  some 
future  date.  Frequently  the  improvement  lasts  many  years  and 
then  a  relapse  comes.  One  of  my  patients  remained  sympto- 
matically  well  more  than  ten  years,  then  died  of  an  acute  thyro- 

125 


126  DISEASES   OF   THE   THYROID   GI^VND 

toxicosis.  The  longer  one  observes  his  patients,  tlie  less  the  per- 
centage of  cures.  One  by  one,  in  the  lapse  of  years,  step  from 
the  cured  group.  I  have  seen  many  patients  operated  on  by 
other  surgeons  who  come  after  several  years  of  improvement 
with  a  relapse.  They  state  that  their  surgeon  does  not  know  of 
their  renewed  trouble.  Therefore,  that  surgeon  has  her  on  his 
records  as  a  cure.  No  doubt  some  of  my  "cures"  are  telling  of 
their  rencAved  trouble  to  some  sympathetic  surgeon. 

It  is  questionable  whether  one  should  ever  speak  of  a  cure. 
Usually  the  whole  gland  is  affected.  Taking  a  part  of  the  bad 
away  does  not  leave  a  good.  It  is  only  in  the  removal  of  fetal 
adenomas  and  the  solitary  cysts  that  we  can  speak  of  a  complete 
cure,  anatomic  and  symptomatic. 

The  best  that  can  be  said  of  the  operative  treatment  is  that 
it  is  the  best  we  have  to  offer  the  patient.  Aside  from  active 
interference  our  efforts  are  not  brilliant;  surgeons  can  well  af- 
ford to  be  truthful  in  their  statements  and  conservative  in  their 
estimates  for  they  alone  can  speak  with  confidence  of  having  ren- 
dered aid.  By  taking  away  a  part  of  the  disease,  the  patient 
can  better  cope  with  the  part  that  remains  than  with  the  whole. 
Fewer  patients  succumb  from  the  operation  than  from  the  dis- 
ease untouched.    Of  this  much  we  may  speak  with  confidence. 

Aside  from  operation  we  can  only  aid  the  patient  in  her 
effort  to  overcome  the  disease.  Much  can  be  done  to  make  the 
struggle  less  uncomfortable.  The  irritation  can  be  lessened,  the 
strength  conserved,  and  the  hope  maintained.  In  the  estimation 
of  cure  by  medical  treatment  one  cannot  separate  the  sponta- 
neous improvement  so  often  noted  from  that  produced  by  the 
exhibition  of  drugs  or  other  curative  means. 

The  best  service  that  can  be  rendered,  therefore,  in  the  dis- 
cussion of  prognosis  is  to  point  out  in  a  general  way  the  usual 
life  histoiy  of  the  disease  and  with  it  the  general  influence  our 
therapeutic  effort  is  apt  to  have.  Such  a  consideration  is  facili- 
tated by  the  discussion  in  turn  of  the  various  types  of  disease. 

Colloid  Goiter. — In  colloid  goiter  much  depends  on  the  age 
of  the  patient  and  the  duration  of  the  goiter. 

Adolescent  Colloid  Goiter. — In  growing  children  the  goiters 
disappear  in  most  cases  after  treatment  with  iodine  in  some 
form.    Many  disappear  spontaneously  it  is  true,  yet  the  influ- 


PROGNOSIS  1 27 

eiice  of  iodine  in  bringing  about  or  expediting  the  result  can- 
not be  doubted.  Some  continue  to  develop,  however,  in  spite  of 
such  treatment,  developing  either  into  large  colloid  or  into  toxic 
goiters. 

Colloid  Goiter  in  the  Adult. — Those  that  disappear  in  early 
life  may  reappear,  most  often  during  a  pregnancy.  Those  that 
remain  from  childhood  and  those  that  appear  in  later  life  may 
persist  unchangeil  for  many  years.  Once  maturity  of  the  indi- 
vidual has  been  reached  there  is  little  tendency  for  the  goiter  to 
disappear,  either  spontaneoush'  or  with  treatment.  The  goiter 
remains  imchanged  in  size  for  many  years.  They  remain  un- 
changed in  size  but  not  unchanged  in  structure.  During  this  so- 
called  innocent  period  changes  in  structure  are  taking  place  as 
indicated  in  the  chapter  on  pathology.  Sudden  hemorrhage  into 
a  cyst  may  as  suddenly  destroy  the  life  of  the  patient.  During 
the  innocent  period  pressure  symptoms  may  harass  her,  injure 
her  lungs  and  damage  her  heart.  If  operated  before  secondary 
symptoms  develop  the  deformity  is  removed.  Just  how  much 
this  contributes  toward  protecting  the  patient  against  mischie- 
vous activity  of  the  remaining  portion  of  the  gland  cannot  be 
stated.  It  will  require  close  observation  of  a  large  series  during 
tlie  period  of  the  patient's  lifetime  to  detennine  this  point. 

Many  of  the  simple  goiters  become  toxic,  slightly  so,  only 
to  subside  again.  Others  repudiate  their  innocence  and  assume 
a  state  of  pronounced  toxicity  requiring  surgical  treatment.  A 
few  develop  into  typical  exophthalmic  goiters  but  the  most  of 
them  present  toxicity  without  exophthalmos.  The  results  of 
surgical  treatment  in  these  cases  are  usually  better  than  the  pri- 
mary toxic  so  far  as  the  control  of  the  toxicity  is  concerned. 
One  can  usually  anticipate  pronouncedly  favorable  results  from 
operation.  The  permanency  of  the  improvement  is  greater  than 
after  operation  on  other  toxic  types. 

If  marked  myocardial  degeneration  has  taken  place,  this  is 
not  restored  by  the  removal  af  the  goiter.  Lung  changes  maj^ 
have  taken  place  and  remain  more  or  less  permanently  damaged. 
The  extent  of  these,  both  before  and  after  operation,  can  be 
but  approximately  determined. 

In  some  of  these  cases  a  more  rapid  degeneration  begins. 
They  lose  markedly  in  weight,  the  heart  previously  damaged. 


128  DISEASES    OF    THE    THYROID   GLAND 

dilates  and  beats  rapidly.  Usually  the  course  goes  uninterrup- 
tedly to  a  fatal  termination.  These  are  the  simple  annals  of  a 
*' simple  goiter."  In  my  experience  a  patient  long  the  host  of 
a  goiter  dies  of  it  sooner  or  later. 

Toxic  Goiter. — Toxic  goiters  vary  much  in  intensity  and  in 
I'apidity  of  onset  and  in  a  measure  on  the  area  of  tissue  involved. 

Fetal  Adenomas. — The  toxic  fetal  adenoma,  without  in- 
volvement of  the  remaining  gland,  rarely  becomes  pronouncedly 
toxic,  shows  little  influence  to  general  measures  and  is  cured 
b}'  removal. 

The  Primary  Toxic  Goiters. — The  life  history  of  the  pri- 
mary toxic  goiter  is  that  of  rapid  ascent,  the  maintenance  of  a 
high  point  for  a  period  of  six  months  to  two  years,  then  a  remis- 
sion. A  recrudescence  often  takes  place.  Complete  recovery  sel- 
dom is  met  with,  but  a  symptomatic  cure  is  not  infrequently 
observed.  In  my  early  practice  it  was  my  privilege  to  observe  a 
considerable  number  of  these  patients  who  ran  their  course  un- 
treated. Manj'  of  these,  now  a  quarter  of  a  century  later,  find 
their  state  tolerable,  many  regard  themselves  as  well.  Those 
that  had  e3'e  signs  have  traces  of  them  still.  There  is  in  some 
a  constantly  rapid  heart,  and  most  are  easily  excited  to  a  mark- 
edly rapid  heart.  A  few  have  died  of  myocardial  degeneration 
with  attendant  dropsy.  Several  whose  disease  began  in  girl- 
hood improved  during  the  child-bearing  years  only  to  suffer  a 
relapse  at  the  menopause.  Only  one  passed  into  a  marked  myx- 
edema. There  remains  usually  a  state  of  nervousness  and  gen- 
eral bodily  lability.  The  hyperacute  cases  usually  terminate  in 
death  in  a  course  of  weeks  or  months.  The  more  chronic  ones 
begin  slowly,  reach  a  state  of  moderate  b:everity,  and  retain  their 
state  for  many  months  or  years  unchanged. 

Such  patients  when  operated  on,  usually  show  a  pronounced 
improvement  beginning  soon  after  operation.  This  is  marked 
first  of  all,  Kocher  pointed  out,  by  a  fall  in  the  lymphocytes. 
The  nervousness  decreases  and  the  weight  begins  to  increase. 
In  the  average  case  this  improvement  continues  and  the  patient 
declares  herself  quite  well,  and  physical  examination  confirms 
her  opinion.  In  many  instances,  however,  the  patient,  if  exam- 
ined, will  be  found  to  still  have  many  of  her  former  symptoms, 
particularly  a  degree  of  rapid  heart;  and  if  there  has  been 


PEOGXOSIS  129 

exoplithalmos,  this  quite  certainly  will  be  found  to  still  persist 
to  some  extent.  Operation  has  accomplished  in  a  month  wliat 
would  have  required  many  years  to  take  place  in  the  natural 
course  of  regression.  What  is  more,  there  is  less  likely  to  be  a 
rapidly  fatal  recrudescence  after  operation  than  after  spon- 
taneous improvement. 

When  improvement  does  not  take  place  after  operation,  one 
of  two  factors  will  be  found  operative.  Either  not  enough  of 
the  gland  has  ])een  removed  or  there  is  some  other  condition 
present  which  cannot  be  influenced  by  operation  on  the  goiter. 
In  the  former  instance  reoperation  is  in  place.  Usually  the 
l^roper  estimate  of  the  amount  of  gland  to  be  removed  will  pro- 
duce a  favorable  result.  One  should  not  hesitate  to  operate  again 
should  it  appear  that  not  sufficient  gland  tissue  has  been  re- 
moved. Not  uncommonly  a  portion  of  the  gland  not  previously 
involved  begins  to  develop  with  a  renewal  of  the  symptoms.  A 
reoperation  will  again  produce  favorable  results  in  these  cases. 
On  the  other  hand,  a  general  nervous  state  or  some  other  source 
of  ill  health  may  underlie  the  complaint.  Whenever  operation 
fails  to  produce  the  desired  result  the  entire  problem  should  be 
studied  again. 

In  some  instances  a  marked  recrudescence  of  the  symptoms 
takes  place  without  any  renewed  increase  in  size  of  the  gland. 
It  is  useless  to  reoperate  for  this ;  it  is  a  degeneration  and  not 
a  proliferation  that  is  causing  the  trouble.  I  have  received  more 
of  these  from  other  surgeons  than  of  my  own  making.  Some  of 
them  die.  Because  of  the  fear  of  such  results  I  seldom  do  a 
complete  bilateral  resection  at  the  first  sitting,  preferring  to 
operate  again  rather  than  face  such  possibilities.  We  know  too 
little  of  the  late  results  of  operation  of  a  bilateral  lobe  resection 
to  follow  this  practice  with  confidence.  These  unfavorable  late 
results  are  more  apt  to  follow  operations  on  patients  with  pro- 
nounced toxicity  who  have  small  goiters.  Generally  speaking, 
the  smaller  the  goiter,  in  proportion  to  the  intensity  of  the  symp- 
toms, the  less  satisfactory  the  results  from  operation. 

Secondary  Degeneration. — The  insidiousness  with  which  a 
toxic  state  may  bo  implanted  on  a  simple  colloid  goiter  has 
already  been  considered.  In  many  of  them  the  toxic  state  devel- 
ops suddenly  and  definitely  resembling  in  symptomatology  the 


130  DISEASES    OF    THE    THYROID   GLAND 

primary  toxic  type.  The  prognosis  is  dependent  almost  wholly 
on  the  degree  of  metabolic  disturbance.  This  is  usually  def- 
initely proportional  to  the  loss  of  weight.  If  the  weight  remains 
stationary  or  begins  to  definitely  increase,  the  operative  prog- 
nosis is  good.  It  is  one  of  the  safest  operations  in  surgery  as  a 
matter  of  fact.  The  symptomatic  results  are  almost  uniformly 
satisfactory  and  the  lingering  symptoms  are  much  less  conspic- 
uous than  after  operation  for  primary  toxic  goiter. 

Those  secondary  goiters  when  they  begin  hyperacutely, 
carry  a  graver  prognosis  than  the  primary  type.  They  carry 
a  greater  operative  risk  and  more  of  them  die  without  treatment. 
The  gravity  is  partly  expressed  by  the  degree  of  emaciation. 
The  addition  of  fever  adds  materially  to  the  gravity  of  the  prog- 
nosis. When  delirium  is  added,  the  outlook  is  very  bad  indeed. 
The  gravity  mounts  as  the  fever  and  delirium  increase.  A  few 
recover,  however,  in  whom  fever  and  delirium  have  developed. 
I  have  never  seen  a  nonoperated  patient  recover  whose  tem- 
perature has  reached  as  high  as  104°. 

These  hyperacute  secondary  toxic  goiters  make  up  by  far 
the  greater  number  of  fatal  cases.  They  are  most  common  in 
old  women  who  have  had  a  goiter  since  young  womanhood.  To 
die  from  such  a  toxic  state  may  be  said  to  be  the  natural  cause 
of  death  in  these  old  goiter  patients. 

Interstitial  Form  (Forme  Fruste). — This  type  does  not  as- 
sume a  severe  form.  The  prognosis  is  more  that  of  the  patient's 
general  condition  and  less  that  of  the  disease.  Sooner  or  later 
the  patients  will  improve  and  resume  the  state  of  health  they  had 
before  the  goiter  manifested  its  activity. 

A  reservation  must  always  be  made  because  the  diagnosis 
is  not  to  be  made  with  certainty  in  many  cases.  What  may 
seem  to  be  a  pure  type  of  this  disease  may  later  show  a  domi- 
nance of  thyroid  disturbance.  That  is,  an  adenoid  disturbance 
becomes  implanted  on  the  interstitial  changes  characteristic  of 
this  type  of  the  disease.  Then  the  prognosis  becomes  that  of 
the  type  and  degree  of  thyroid  disturbance  presented.  If  the 
adenoid  disturbance  is  markedly  dominant,  much  may  be  ex- 
pected from  operation. 

Not  much  can  be  expected  from  operation  in  the  pure  inter- 
stitial type  because  the  thyroid  gland  usually  represents  but  a 


PROGNOSIS  131 

part  of  the  disease.  There  is  commonly  a  pelvic  disturbance 
that  is  not  amenable  to  treatment.  The  results  to  be  expected 
from  operation  may  be  judged  by  the  state  of  the  patient's 
health  before  the  goiter  developed.  One  cannot  hope  to  exceed 
this  state.  I  hesitate  to  operate  on  these  patients  because  they 
seldom  receive  the  benefit  they  expect.  I  have  seen  a  number  of 
these,  who  have  been  operated  on  by  surgeons  of  the  highest 
standing,  made  worse  by  the  operation.  Man}'  of  these  receive 
temporary  improvement,  it  is  true,  following  operation,  but  they 
quite  as  regularly  lapse  into  their  former  state  sooner  or  later. 
It  is,  therefore,  the  selection  of  the  case  and  not  the  technical 
skill  that  was  at  fault. 

Malignancy 

There  are  those  who  speak  of  curing  malignancy  of  the 
thyroid.  Our  knowledge  of  histopathologic  diagnosis  is  not  yet 
exact  enough  to  permit  us  to  speak  positively  in  many  cases. 
When  we  have  to  do  with  suspected  malignancy  we  may  be 
pretty  sure  that  either  our  diagnosis  is  wrong  or  there  will  be 
a  recurrence.  It  is  too  much  to  expect  that  we  may  cure  a  con- 
dition where  we  do  little  more  than  remove  the  suspected  lesion 
with  little  attention  to  the  environment.  Much  less  may  we 
credit  those  cases  where  a  resection  of  the  malignant  gland  is 
alleged  to  have  produced  a  cure.  In  those  cases  in  which  a  diag- 
nosis can  be  positively  made,  I  refuse  operation.  The  suspected 
cases  that  remain  well  after  operation  one  may  be  fairly  sure 
were  not  malignant. 

Mortality  after  Operation 

The  operative  risk  in  colloid  goiter  comes  from  pneumonia, 
tracheal  collapse,  hemorrhage  and  infection.  Each  of  these  are 
factors  of  the  rarest  occurrence.  There  are  few  diseases  of 
like  magnitude  in  which  the  operative  prognosis  is  so  good.  In 
long  existing  cases  the  heart  may  become  much  affected  and  this 
may  invite  complications,  but  heart  failure  per  se  is  but  little 
to  be  feared  following  operation  for  simple  goiter.  Hemorrhage 
and  infection  can  be  prevented  as  certainly  as  anything  in  sur- 
gery.    Tracheal  collapse  is  rarely  troublesome  and  pneumonia 


132  DISEASES    OF    THE    THYROID   GLAXD 

following  operations  under  local  anesthesia  is  a  disaster  wholly 
foreign  to  my  experience. 

In  the  toxic  type  the  risk  is  directly  proportionate  to  the 
degree  of  metabolic  disturbance.  In  extreme  emaciation  or  in 
the  presence  of  a  rise  of  temperature  the  risk  is  definite  despite 
every  care  the  surgeon  may  invoke.  The  risk  from  operation  is 
greater  than  from  expectant  treatment.  One  should  wait  for  a 
remission  and  then  operate. 

There  is  no  disease  that  is  so  largely  dependent  on  the  skill 
and  judgment  of  the  surgeon.  Everj^  operative  death  must  be 
regarded  as  an  impeachment  of  his  ability  and  should  be  a  signal 
for  the  careful  reconsideration  not  only  of  the  factors  under- 
lying the  case  in  question  but  also  of  his  whole  viewpoint  of 
the  disease.  To  justify'  itself,  operation  for  goiter  must  be  with- 
out mortality. 

It  is  interesting  to  note  that  while  the  technics  of  the  vari- 
ous operators  differ  nmch  in  detail,  some  simple,  some  elaborate, 
the  operative  prognosis  is  about  the  same.  It  seems  fair  to  pre- 
sume, therefore,  that  the  determining  factor  is  skill  in  operating, 
born  of  experience,  and  not  any  particular  procedure,  that  counts 
in  the  operative  results. 


CHAPTER  VI 

GOITERS  IN  UNUSUAL  PLACES 

Under  this  head  may  be  grouped  all  those  conditions  which 
because  of  their  topograpliic  relationsliip  cause  some  disturb- 
ance by  virtue  of  such  location.  For  the  most  part  they  do  tliis 
mischief  as  tumors  and  the  goitrous  element  is  unimportant  or 
incidental.  Tlie  most  common  conditions  to  be  considered  are 
those  in  Avhich  the  trachea  is  displaced  or  compressed  by  the  ab- 
normal expansion  of  the  gland.  Next  in  frequency  come  the 
growths  into  or  extension  into  areas  not  normally  occupied  by 
the  thyroid  gland.  These  comprise  the  substernal,  in  which  the 
lower  pole  grows  into  the  thoracic  cavity  leaving  a  part  only  to 
occupy  the  normal  situation  of  the  gland,  then  the  intrathoracic 
goiters  in  Avhicli  tlie  entire  enlargement  lies  within  the  thorax, 
leaving  no  part  of  the  enlargement  at  the  normal  site  of  the 
gland.  Next  are  the  aberrant  goiters  which  from  some  trick 
of  development  remain  at  some  unusual  situation.  These  lie 
usually  at  the  angle  of  the  jaw  or  at  the  base  of  the  tongue. 
Finally  the  intratracheal  goiters,  though  rare,  deserve  consid- 
eration. 

Abnormal  Expansion  of  the  Normally  Situated  Thyroid  Gland 

Under  this  awkward  heading  all  those  conditions  in  which 
the  expanding  gland  produces  mischief  may  be  grouped.  The 
gradual  s}mimetrical  growth  of  both  lobes  may  compress  the 
trachea  between  them  (Fig.  59).  This  is  most  likely  to  happen 
in  old  calcareous  goiters.  This  compression  flattens  the  trachea 
so  that  it  becomes  a  mere  slit  giving  rise  to  the  old  expression 
"saber  sheath"  trachea.  If  one  lobe  expands  chiefly  the  trachea 
may  be  widely  displaced  or  displaced  and  compressed.  Some- 
times secondary  or  irregular  bosselations  may  produce  unusual 
conditions.  The  most  common  are  those  in  which  a  nodule 
grows  medially  between  the  trachea  and  esophagus  (Fig.  60). 
Hemorrhage  into  a  cavity  remaining  after  the  removal  of  such 

133 


134 


DISEASES    OF    THE    THYROID   GLAND 


Fig.  59. — The  trachea  is  shown  as  being  compressed  between  the  lobes  of  the  goiter 
producing  the  so-called  sword-sheath  trachea.  /,  the  trachea  being  compressed  by  bilateral 
lobe  enlargement;  la,  the  same  showing  in  cross  section  the  result  of  such  compression;  2, 
the  trachea  is  shown  as  being  both  compressed  and  displaced  by   unequal   lobe   hypertrophy. 


Fig.  60. — Diagram  showing  the  manner  in  which  a  lobe  may  grow  between  the  trachea 
and  esophagus,  compressing  both  these  tubes.  The  right  recurrent  nerve  lies  in  a  groove 
between   the  right  and   the  aberrant  lobes. 


GOITERS   IX    UXUSUAL   PIACES 


135 


a  lobe  may  cause  sudden  deatli  by  compression  of  the  trachea 
(Fig.  61)/    . 

Compression  of  the  Trachea. — The  effect  of  the  compres- 
sion of  the  trachea  may  be  dyspnea  or  secondary  affections  of 
the  lungs.  Often  the  dyspnea  is  facultative;  that  is  to  say,  in 
certain  positions  the  patient  has  difficulty  in  breathing,  in  others. 


Fig.  61. — Photograph  of  a  specimen  in  which  the  rounded  lobe  on  the  right  lay  between 
the  trachea  and  the  esophagus  producing  dyspnea  and  dysphasia.  Secondary  hemorrhage  into 
the   cavity   occupied   by  this   lobe   produced   dangerous   tracheal   obstruction   after   the   operation. 

not.  This  is  particularly  noted  when  the  patient  is  in  bed.  The 
jdllows  must  be  arranged  in  a  particular  way.  When  sudden 
changes  take  place  in  the  gland,  the  situation  may  be  more  seri- 
ous. 

Compression  of  the  Vessels. — Besides  the  tracheal  compres- 
sion, the  neighboring  vessels  may  be  compressed,  producing  sec- 


ISfD 


DISEASES    OF    THE    THYROID   GLAXD 


oiidaiy  affections  of  the  lieart.  Though  it  is  well  established  in 
ihe  literature,  in  iny  experience  the  degree  of  cardiac  disturb- 
ance bears  no  or  at  least  very  little  relation  to  the  degree  of  dis- 
turbance of  the  circulation.  It  is  just  as  easy  to  believe  the 
"innocent"  goiter  has  gradually  poisoned  the  heart. 


Fig.    62. — X-ray   picture   showing   the    trachea    pushed    far   to    the    left    by    a    medial   lying   sub- 
sternal goiter.     The  trachea  is  represented  by  a  broad  light  band  to  the  right  of  the  picture. 


Dysphasia. — Difficulty  in  swallowing  is  sometimes  com- 
plained of  by  goiter  patients.  Only  occasionally  is  there  an  ac- 
tual impingement  on  the  esophagus.  In  most  cases  the  sense  of 
constriction  is  a  nervous  manifestation. 

Compression  of  the  Nerves. — Compression  on  the  surround- 


GOITERS    IX    UNUSUAL   PLACES  137 

ing  nerves  is  frequently  noted.  In  large  old  goiters  there  is 
often  a  paralysis  of  one  of  the  vocal  cords.  This  may  be  indi- 
cated by  the  disturbance  of  the  voice,  but  it  is  usually  not  so 
announced.  The  vocal  apparatus  should  be  examined  in  each 
case  lest  the  discovery  of  it  after  operation  might  lead  to  the 


Fig.  63. — X-ray  of  a  goiter  iti  which  the  calcareous  plaiiue  caused  misjudgment  as  to  the  loca- 
tion of  the  trachea.  The  light  area  at  the  extreme  top  of  the  picture  was  taken  to  be  the 
trachea.      This   was   a   calcareous    deposit   and    the    trachea   was   found    displaced    far   to    the    left. 

opinion  that  the  paralysis  was  due  to  the  operation.  A  knowl- 
edge of  its  presence  before  operation  would  be  a  source  of  satis- 
faction to  the  surgeon  in  case  of  a  damage  suit,  but  it  is  a  ficti- 
tious hope  that  such  a  record  would  have  any  influence  on  the 
court  or  jury. 


138  DISEASES    OF    THE    THYROID   GLAND 

One  of  the  sympathetic  nerves  is  sometimes  compressed 
producing  dilatation  of  the  pupil  on  the  affected  side. 

Not  uncommonly,  pain  in  the  mastoid  region  is  complained 
of,  caused  by  compression  of  the  deep  sensory  nerves  of  the 
neck. 

Diagnosis. — The  recognition  of  disturbances  caused  by  the 
abnormal  development  of  goiters  is  not  always  easy.  Usually 
the  displacement  of  the  trachea  can  be  readily  palpated  or  it 
may  be  demonstrated  by  the  x-ray  (Fig.  62).  Sometimes  when 
the  gland  is  hard  and  calcareous,  neither  of  these  means  is  of 
help  (Fig.  63).  In  such  cases  the  laryngoscopic  examination  may 
show  a  narrowing  of  the  trachea.  In  some  cases  one  cannot 
prove  that  a  narrowing  of  the  trachea  exists,  but  there  being  a 
goiter  and  dyspnea  the  one  may  be  assumed  to  have  followed 
the  other.  Other  possible  causes  of  dyspnea,  of  course,  must  be 
kept  in  mind  lest  the  patient  be  disappointed  if  the  operation 
does  not  relieve  the  symptoms. 

Nerve  compressions  when  coexistent  with  the  goiter  may 
be  assumed  to  be  due  to  it  but  other  causes  for  the  condition 
should  always  be  excluded. 

The  importance  of  a  careful  diagnosis  of  the  conditions 
here  considered  lies  in  the  fact  that  especial  caution  is  required 
in  the  preparation  for  the  operation.  Those  particularly  who 
operate  under  general  anesthesia  will  do  well  to  have  a  trache- 
otomy tube  at  hand  and  to  locate  the  trachea  as  early  as  pos- 
sible after  the  operation  is  begun.  Further  details  may  be  found 
in  the  chapter  on  technic. 

Substernal  and  Intrathoracic  Goiter 

Strictly  speaking,  an  enlargement  of  the  thyroid  gland  is 
a  *' goiter"  (that  is  to  say  a  ''big  neck")  only  when  it  is  situ- 
ated in  the  normal  position.  However  as  is  so  often  the  case, 
inaccuracy  is  most  expressive,  for  in  the  more  common  type,  the 
substernal,  the  displaced  portion  migrated  because  of  the  pres- 
sure from  the  "goiter"  above.  Therefore,  while  physiologically 
incorrect,  it  expresses  the  pathogenesis  very  well  so  far  as  it 
concerns  the  substernal  but  the  intrathoracic  cannot  be  so  ex- 
plained. The  thyroid  gland  is  situated  just  above  the  superior 
opening  of  the  thorax.    It  follows  naturally  that  if  a  certain  de- 


GOITERS    IN    UNUSUAL   PLACES 


139 


gree  of  enlargement  is  surpassed,  tlie  projecting  poles  must 
needs  enter  the  thoracic  cavity.  AVhen  this  takes  place,  that  por- 
tion projecting  into  the  thoracic  cavity  is  called  substernal  or 
if  located  to  one  side,  retroclavicular.  The  extension  from  above 
downwards  usually  involves  the  lateral  lobes  and  consequently 
the  displaced  portion  may  be  located  to  one  or  the  other  side. 
However,  since  the  midline  offers  the  least  resistance,  usually 
no  matter  from  which  lobe  they  arise,  they  tend  to  reach  the 
midline  (Fig.  64). 


Fig.  64. — Diagram  showing  the  difference  between  a  substernal  and  an  intrathoracic  goiter. 
I,  Substernal,  being  a  prolongation  into  the  thorax  of  a  normally  situated  goiter,  and,  2,  an 
intrathoracic  being  attached  to  the  isthmus  by  a  fibrous  cord  only. 

In  those  instances  in  w^hich  the  whole  enlargement  lies 
within  the  thoracic  cavity,  without  there  being  any  goiter  in  the 
neck,  they  are  then  called  intrathoracic,  for  they  are  actually 
so.  Kleinbock  (Med.  Klin.,  1908,  iv,  488-495)  divides  the  intra- 
thoracic goiters  again  as  to  their  relation  to  the  vessels  of  the 
neck.  When  they  lie  laterally  they  are  situated  between  the 
vertebral  column  and  esophagus  behind,  lateral  to  the 
trachea,  medial  to  the  apical  pleura  and  behind  the  common 
carotid  and  anonymous  arteries  and  their  veins.  The  medial 
intrathoracic  goiter  lies  in  front  of  the  large  vessels  and  in  front 


140  DISEASES    OF    THE    THYROID   GLAND 

of  or  inniiediatoly  to  one  side  of  tlie  trachea.  In  front  is  the 
sternum  and  below,  tlie  arch  of  the  aorta.  Generally  speaking, 
those  derived  from  the  lateral  lobes  lie  behind  the  vessels,  those 
arising  from  the  isthmus  lie  in  front.  AVhether  they  come  to  lie 
substernally  because  of  accident  of  growth  or  developmental 
anomalies  is  not  always  clear.  Some  are  attached  to  the  re- 
mainder of  the  gland  by  a  narrow  pedicle  when  the  remainder  of 
the  gland  is  normal  in  size  and  situation.  In  addition  these 
nodules  are  ovoid  in  form  and  the  attaching  pedicle  reminds  one 
forcibly  of  the  aberrant  goiters  in  other  situations.  This  type, 
it  is  fair  to  assume,  are  really  aberrant  goiters  and  in  contra- 
distinction to  the  following  may  be  called  primary  intrathoracic. 
The  secondary  type  is  usually  attached  to  a  lateral  lobe,  gener- 
ally by  a  broad  pedicle.  However,  the  primary  intrathoracic 
type  is  attached  to  one  of  the  lower  poles  and  its  definite  pedicle 
often  a  direct  extension  of  the  isthmus.  Lahey  (Jour.  Am. 
Med.  Assn.,  1920,  Ixxv,  163)  has  recently  emphasized  the  fact 
that  a  substernal  goiter  may  become  an  intrathoracic  one  if  the 
mass  is  pear-shaped.  As  it  grows  in  size,  its  wedge  shape  pulls 
it  down,  like  a  growing  uterus  pulls  itself  up  into  the  abdomen. 
Those  in  contradistinction  to  the  preceding  may  be  called  sec- 
ondary intrathoracic  goiters. 

Some  goiters  have  the  faculty  of  spending  a  part  of  the  time 
above  the  sternum  and  part  beneath  it.  These  are  called  wan- 
dering goiters.  They  sometimes  can  be  made  to  appear  at  will 
by  coughing.  As  they  grow  larger,  they  can  no  longer  be  ex- 
pelled and  they  remain  permanently  behind  the  sternum,  or  com- 
monly they  remain  above  the  clavicle.  I  had  one  patient  who 
wore  the  goiter  above  the  clavicle  when  about  her  household 
duties,  but  pushed  it  below  the  clavicle  when  she  went  out  into 
society.  She  nearly  died  in  a  fit  of  coughing  at  a  social  function. 
She  then  had  it  removed. 

Incidence. — Substernal  goiters,  those  that  are  for  the  most 
part  above  the  sternum  and  extend  below  only  in  part,  are  quite 
common  in  colloid  goiters,  being  so  in  about  one-fourth  of  the 
cases.  Intrathoracic  goiters  are  much  less  common,  represent- 
ing not  more  than  a  fourth  per  cent  of  all  goiters.  This  type  is 
nmcli  less  frequent  in  primary  toxic  goiters  and  in  typical  Base- 
dow patients.    I  have  seen  a  number  in  which  the  entire  enlarged 


GOITERS    IX    ITXUSI^4L   PLACES 


141 


lobe  was  liidden  beneatli  tlie  sternum.  Xot  infrequently  toxic  goi- 
ters are  pear-sliaped  with  the  big  end  of  the  pear  nested  in  the 
supra-clavicular  fossa,  while  the  gland  in  the  normal  situation 
seems  but  little  enlarged.    This  type  occurs  in  some  5  per  cent  of 


Fig.    65. — This    patient    had    a   typical    exophthalmic    goiter    with    no    apparent    thyroid    enlarge- 
ment.    The   goiter    lay    behind    the    sternum. 


cases.  One  is  apt  to  regard  these  as  '^ Graves'  disease  without 
goiter"  (Fig.  65),  unless  one  uncovers  the  prolonged  pole  by 
operation.    Both   the  substernal   and  intrathoracic   occur  most 


142  DISEASES    OF    THE    THYROID   GLAND 

frequently  in  midlife  or  beyond,  most  likely  because  the  larger 
goiters  appear  in  more  advanced  years.  However,  I  have  seen 
the  substernal  as  early  as  seventeen  years  and  the  intrathoracic 
at  the  age  of  twenty-two.  The  intrathoracic  are  said  to  occur 
most  frequently  in  the  male,  a  statement  entirely  in  accord  ^s^-itli 
my  own  experience. 

Symptoms. — The  disturbances  caused  by  abnormally  sit- 
uated thyroid  lobes  are  dependent  almost  entirely  upon  the 
mechanical  displacement  of  organs  native  to  this  region.  These 
are  the  trachea,  the  esophagus,  the  blood  vessels,  and  the  nerves. 
The  sjTiiptoms  do  not  differ  materially  from  those  already  de- 
tailed for  compression  by  the  normally  situated  goiters.  Herein 
lies  the  importance:  one  may  think  he  has  removed  the  cause  of 
the  trouble  when  the  normally  situated  goiter  has  been  re- 
moved, yet  the  chief  trouble  may  lie  within  the  thorax. 

The  trachea  is  naturally  in  most  intimate  contact  with  the 
goiter  and  any  considerable  compression  of  it  is  registered  by  a 
lessened  facility  of  the  interchange  of  air.  Dyspnea  may  be  pro- 
duced either  by  compression  or  displacement.  Often  this  dyspnea 
develops  so  gradually  that  there  may  be  no  objective  evidence  of 
it  and  the  obstruction  may  reach  a  considerable  degree  before 
the  patient  registers  complaint,  just  as  in  the  normally  situated 
goiter.  Because  of  the  change  in  position  of  the  tumors  and 
trachea  by  the  different  position  of  the  head,  the  dyspnea  may 
be  increased  or  lessened  by  holding  the  head  in  a  certain  posi- 
tion. It  is  indicative  of  this  type  of  the  substernal  goiter  if  ele- 
vating the  chin  or  depressing  it  or  holding  it  to  one  side  in- 
creases or  lessens  the  respiratory  difficulty.  Therefore,  if  the 
patient  desires  high  pillows  or  is  compelled  even  to  maintain  a 
sitting  position,  a  substernal  lobe  likely  exists.  If  change  of 
position  makes  no  difference,  one  should  think  of  an  intrathor- 
acic lobe. 

Disturbances  of  deglutition  are  much  less  conmion  than  dis- 
turbances of  respiration,  because  the  esophagus  glides  out  of  the 
way  more  easily  and  its  patency  is  not  an  unremittent  neces- 
sity. When  this  is  present,  either  the  tumor  is  very  large  or  a 
smaller  lobe  is  insinuating  itself  between  the  trachea  and  esoph- 
agus. Disturbance  of  deglutition  is  most  apt  to  occur  in 
the  retrovascular  type.    Occasionally  the  disturbance  is  so  great 


GOITERS    IX    UNUSUAL   PLACES  143 

as  to  simulate  a  malignant  i^rocess,  but  it  usually  is  only  marked 
enough  to  excite  the  attention  of  the  patient  sufficiently  to  make 
it  a  matter  of  record. 

The  patient  may  be  harassed  by  a  constant  cough.  This 
may  be  due  to  a  direct  irritation  of  the  trachea,  but  more  often 
is  caused  by  displacing  or  compressing  the  recurrent  laryngeal 
nerve.  Occasionally  the  "goose  cough"  due  to  recurrent  irri- 
tation gives  the  first  clue  to  the  nature  of  the  trouble  and  sug- 
gests an  intrathoracic  goiter.  Not  infrequently  there  is  a 
paralysis  of  a  cord  without  the  patient's  being  aware  of  any  dif- 
ficulty of  any  sort.  A  laryngoscopic  examination,  therefore, 
should  always  be  made  when  a  hidden  goiter  is  suspected. 

Usually  compression  of  the  veins  causes  a  dilatation  of  the 
superficial  veins  over  the  sternum  and  the  base  of  the  neck.  Less 
common  pressure  on  the  anonymous  artery  may  produce  an  in- 
equality of  the  pulse.  Swelling  of  the  face  and  edema  of  the 
arm  have  been  noted  (Bard:  Rev.  med.  de  la  Suisse,  1905,  xxv, 
204). 

Diagnosis. — ^Wlien  there  is  dyspnea  with  the  presence  of 
a  goiter  in  the  neck,  in  the  absence  of  other  causes,  compression 
of  the  trachea  may  be  assumed.  When  there  is  a  goiter  in  the 
usual  situation,  one  should  first  determine  whether  this  is  com- 
pressing the  trachea.  If  not,  a  substernal  goiter  must  be  sought. 
A  deviation  of  the  trachea  may  be  palpated  and  if  not  accounted 
for  by  the  normally  situated  goiter,  suggests  a  prolongation 
into  the  thorax.  When  such  can  be  demonstrated,  the  diagnosis 
is  usually  completed.  There  are  exceptions.  I  once  examined 
a  patient  who  had  had  a  goiter  for  many  years.  She  developed 
a  dyspnea,  and  a  substernal  tumor  apparently  continuous  with 
the  goiter  was  demonstrated  by  the  x-ray.  The  substernal  tumor 
proved  to  be  a  metastatic  carcinoma  from  a  breast  removed 
many  years  before. 

When  there  is  narrowing  of  the  trachea  the  question 
arises  whether  this  is  due  to  compression  by  the  normally  sit- 
uated goiter  or  to  pressure  of  an  abnormally  situated  lobe. 
Sometimes  displacement  of  the  trachea,  shown  by  palpation 
or  by  the  x-ray,  not  accounted  for  by  the  size  and  situ- 
ation of  the  goiter  in  the  neck  gives  a  clew.  Under  favorable 
conditions  the  laryngoscope  will  reveal  the  actual  situation  of 


144  DISEASES    OF    THE    THYROID   GLAND 

the  narrowing.  Percussion  of  the  upper  end  of  the  sternum  will 
show  dullness  if  the  displaced  lobe  be  large.  The  larynx  may 
not  make  the  usual  excursions  in  deglutition  and  it  may  be  sit- 
uated abnormally  low.  Both  these  signs  are  significant.  The  x- 
ray  is  the  most  valuable  aid  in  showing  the  presence  of  a  tumor 
of  the  upper  mediastinum.  It  is  most  valuable  when  the  gland  is 
old,  particularly  if  it  contains  calcified  areas.  The  x-ray  usually 
adds  valuable  evidence,  but  it  may  also  mislead.  I  have  failed 
to  find  substernal  goiter  when  the  x-ray  seemed  to  indicate  its 
presence  and  more  often  I  have  found  it  when  the  plate 
showed  no  shadow.  If  a  shadow  can  be  detected  under  the 
sternum  by  means  of  the  fluoroscope  and  this  shadow  moves  with 
the  trachea  with  deglutition,  the  diagnosis  is  certain.  The 
surgeon  should  verify  this  evidence  whenever  possible,  how- 
ever. Mobility  may  be  reported  from  the  x-ray  laboratory  when 
none  exists.  The  play  of  shadows  during  deglutition  is  often 
confusing  and  slight  changes  may  be  magnified  by  those  who  are 
not  to  assume  the  responsibilit}'  of  the  operative  procedure. 
Sometimes  the  tumor  itself  prevents  this  excursion.  This  occurs 
usually  in  tumors  of  large  size  or  those  fixed  by  secondary 
changes.  Generally  speaking,  all  the  factors  must  be  taken  to- 
gether before  a  conclusion  is  hazarded  and  then  the  surgeon 
should  approach  the  operation  with  the  feeling  that  the  opera- 
tion alone  can  clear  up  the  final  doubt. 

Interference  of  deglutition  is  less  valuable  as  evidence  than 
is  disturbance  of  the  trachea.  Its  presence  without  evidence 
of  respiratory  disturbance  should  cause  one  to  proceed  with 
caution.  I  was  once  sent  a  patient  for  the  removal  of  a  suppo- 
sitious substernal  goiter  which  it  was  alleged  was  responsible 
for  a  dysphasia.  The  x-ray  had  demonstrated  its  presence,  it 
was  said.  As  I  approached  the  patient,  already  on  the  operating 
table,  he  burst  out  weeping.  Since  patients  do  not  usually  Aveep 
so  copiously  on  making  my  acquaintance,  I  retired  and  signaled 
a  neurologist.    A  diagnosis  of  bulbar  paralysis  was  made. 

The  diagnosis  of  intrathoracic  goiter  is  much  more  difficult 
than  the  recognition  of  the  substernal.  They  are  missed  because 
one  does  not  think  of  .the  possibility  of  their  presence.  Some- 
times cough  is  the  chief  or  only  sign.  Since  intrathoracic 
goiters  are  most  common  in  the  emphysematous,  one  may  pass 


GOITERS    rX    UXT'SUAL    PLACES  145 

over  this  complaint  lightly.  The  goiter  by  pressure  on  the 
trachea,  or  in  rare  instances  on  the  bronchi,  may  add  materially 
to  the  emphysema.  In  such  cases  emphysema  may  exist  with- 
out the  classical  barrel-shaped  chest  commonly  associated  with 
this  syndrome  and  thus  give  a  clew.  Extensive  emphysema  may 
obliterate  substernal  dullness.  As  a  matter  of  fact,  substernal 
dullness  is  a  sign  of  uncertain  value  because  of  the  associated 
changes  above  noted.  Wohrmann  (Deutsch.  Ztschr.  f.  Chir., 
1906,  xliii)  was  able  to  demonstrate  it  in  but  10  of  75  cases.  This 
corresponds  to  my  experience.  The  dilatation  of  the  veins  of 
the  skin,  referred  to  as  a  sign  of  substernal  goiter,  may  be  some- 
what vitiated  by  a  generalized  phlebectasis  of  the  chronic 
asthmatic.  In  such  cases  the  study  of  the  excursions  or  the 
position  of  the  trachea  ag  it  disappears  into  the  thorax  may  be 
of  the  greatest  value.  Its  deviation  from  the  midline  often  is 
a  hint  of  great  value.  Sometimes  a  finger  placed  in  the  supra- 
sternal notch  may  receive  an  impulse  when  the  patient  swallows 
or  coughs.  A  pulsation  on  coughing  in  the  supraclavicular 
space  once  enabled  one  of  my  assistants  (Olsen)  to  catch  the 
clew  after  I  had  gone  over  the  patient  repeatedly  and  found 
nothing  but  a  recurrens  paralysis  (Fig.  66).  Only  after  all  the 
signs  have  been  carefully  studied  should  an  opinion  be  hazarded. 
In  rare  instances  the  presence  of  the  usual  symptoms  of  toxic 
goiter  without  there  being  any  goiter  visible  will  lead  to  the  suc- 
cessful search  for  one  behind  the  sternum. 

When  the  intrathoracic  goiter  becomes  malignant  shooting 
pains  and  bloody  sputum  are  added  to  the  usual  picture.  Fixa- 
tion of  the  trachea  is  apt  to  be  absolute,  and  deglutory  disturb- 
ances progress  rapidly.  Metastatic  mediastinal  masses  from 
goiters  normally  situated  sometimes  occur.  In  the  only  instance 
of  this  kind  in  my  experience,  the  normally  situated  goiter,  be- 
cause of  its  hardness  and  fixity,  was  obviously  malignant,  and 
since  the  mediastinal  symptoms  were  of  recent  origin,  a  second- 
ary relation  was  probable.  The  x-ray  showed  not  only  a  tumor 
in  the  mediastinal  space,  but  others  in  the  lungs  thus  settling 
the  small  element  of  doubt  that  remained. 

Hemorrhage  into  a  substernal  goiter  may  suddenly  increase 
the  volume  of  the  tumor.    One  of  my  patients,  known  to  have  a 


146 


DISEASES    OF    THE    THYROID   GLAND 


substernal  goiter,  suffocated  during  a  night  from  what  was  prob- 
ably a  hemorrhage  into  the  tumor. 

When  a  mediastinal  tumor,  supposedly  goitrous,  has  been 


Fig.  66. — Intrathoracic  goiter  in  a  patient  with  dysphagia  and  cough.  The  goiter  lies  sub- 
sternal. During  efforts  at  coughing  it  could  be  seen  bulging  behind  the  left  sternoclavicular 
articulation. 

hypothecated,  a  differentiation  from  other  mediastinal  growths 
must  be  made. 

Thymus  tumors  have  been  observed,  but  are  rare.    In  the 


GOITERS    IX    UNUSUAL   PLACES  147 

adult  they  are  usually  malignant  and  the  duration  is  less  than 
in  intrathoracic  goiters.  The  trachea  is  less  apt  to  be  compressed 
and  is  usually  neither  displaced  nor  fixed.  Lymphosarcomas  are 
the  commonest  mediastinal  tumors.  They  often  show  dullness 
on  percussion  and  the  x-ray  shows  them  some  distance  below 
the  sternal  notch.  The  top  is  more  rounded  and  does  not  ex- 
tend up  so  high.  The  trachea  is  not  fixed  until  late  and  then 
there  are  usually  several  tumors  present.  Sometimes  there  are 
lymphomas  elsewhere.  Metastatic  tumors,  from  primary  tu- 
mors situated  at  a  distance,  are  sometimes  encountered.  Sar- 
comas are  the  most  common.  Usually  there  is  no  difficulty  in 
discovering  the  primary  tumor,  but  sometimes  the  patient  does 
not  volunteer  the  information.  Aneurysm  is  usually  sufficiently 
demonstrated  by  the  x-ray.  It  is  interesting  to  know  that  a 
goiter  may  pulsate,  but  it  is  not  the  expansile  pulsation  of 
aneurysm  and  there  is  no  bruit.  Goiters  may  disturb  the  syn- 
chronicitj^  of  the  carotids  or  the  two  radials.  Usually  too,  intra- 
thoracic goiters  are  encountered  at  an  age  when  aneurysms  are 
not  found,  that  is  to  say,  beyond  fifty  years.  Still  rarer  tumors 
are  sometimes  encountered.  I  once  encountered  a  substernal 
dermoid.  It  presented  in  the  sternal  notch,  was  semifluctuant 
and  did  not  disturb  the  excursions  of  the  trachea.  Lipomas  are 
rare  substernal  tumors,  and  usually  do  not  occupy  the  upper 
mediastinal  space  alone. 

Treatment. — Once  a  substernal  or  intrathoracic  goiter  has 
caused  the  patient  trouble,  it  must  be  removed.  The  substernal 
goiters  give  but  little  trouble  because  the  suprasternal  portion 
gives  a  good  handle  and  furnishes  a  good  guide.  All  that  is 
needed  is  the  careful  determijiation  of  the  line  of  cleavage.  This 
found,  one  can  raise  the  offending  mass  by  gentle  traction.  For- 
tunately the  vessels  supplying  it  have  gone  do\\Ti  with  the  pro- 
gressive development  of  the  lobe  and  as  it  is  withdrawn  the 
vessels  become  more  accessible.  It  is  only  when  the  submerged 
lobe  is  very  large  that  it  is  necessary  to  reduce  the  size  by  evis- 
ceration. This  is  best  done  by  exposing  the  top  of  the  tumor, 
which  can  usually  be  done  by  making  a  long  transverse  incision 
just  above  the  sternum,  separating  the  sternal  insertions  of  the 
clavicle  if  necessar}^,  making  an  incision  into  the  goiter  and  by 
grasping  the  capsule  with  forceps  it  can  be  held  while  the  finger 


148  DISEASES    OF    THE    TIIVROID   GLAND 

scoops  out  the  colloid  material  within.  By  continued  traction 
and  the  scooping  manipulation  the  mass  can  be  brought  forth. 
As  the  vessels  entering  the  gland  appear  they  should  be  caught 
and  ligated.  By  this  technic  I  have  removed  a  mass  as  large 
as  two  fists.  Should  the  capsule  be  calcified,  new  difficulties 
would  be  encountered  because  in  addition  to  being  incollapsible 
there  would  likely  be  a  firm  union  with  the  trachea.  Jacques  and 
Michel  (Rev.  med.  de  I'st  Nancy,  1910,  xiii,  233)  report  a  calci- 
fied intrathoracic  goiter.  Fortunately  the  size  of  the  tumor  was 
not  great  enough  to  offer  difficulties.  Retrosternal  goiters  not 
infrequently  have  calcified  areas.  These  can  be  crushed  and  de- 
livery effected.  This  can  usually  be  done  without  exciting  any 
considerable  hemorrhage. 

The  substernal  masses  sometimes  lie  so  deeply  that  they 
are  difficult  to  grasp.  Sometimes  if  the  patient  coughs  violently, 
the  gland  may  be  so  much  elevated  that  it  maj  be  grasped.  A 
husky  ranchman  once  aided  me  by  this  means.  The  gland  was 
so  deeply  situated  that  I  could  not  grasp  it.  A  violent  cough, 
made  at  my  request,  fairly  shot  the  offending  lobe  up  into  the 
neck  and  it  remained  perched  above  the  sternoclavicular  articu- 
lation and  its  removal  was  effected  with  the  greatest  ease. 

In  exceptionally  difficult  cases,  the  natural  avenue  of  ap- 
proach is  not  sufficient.  I  have  employed  a  lateral  method  of  ap- 
proach by  removing  the  costochondral  cartilage  of  the  first  and 
second  ribs  and  then  biting  away  the  adjacent  sternmn  with  a 
ronguer.  This  gives  good  access  to  the  gland.  However,  I  be- 
lieve Milton's  method,  which  consists  of  the  longitudinal  split- 
ting of  the  sternum  as  employed  by  Lilienthal  (Surg.  Gynec.  and 
Obst.,  1915,  p.  389)  is  preferable  in  some  respects  in  that  it  gives 
better  access  to  the  lower  extremity  of  the  tumor.  In  any  of 
these  very  difficult  cases  it  is  well  to  remember  that  if  the  hem- 
orrhage becomes  threatening  it  is  best  to  pack  with  gauze  and 
finish  at  another  sitting. 

When  the  apparent  cause  of  tracheal  obstruction  has  been 
found,  one  must  assure  himself  that  the  whole  trouble  has  been 
relieved.  I  once  came  near  overlooking  an  intrathoracic  lobe 
after  a  substernal  one  had  been  removed.  One  patient  had  been 
operated  on  and  an  enlarged  right  lobe  with  a  prolonged  lobe 
extending  well  behind  the  clavicle  had  been  removed.    I  found 


GOITERS    I^ST    UN^USUAL   PLACES 


149 


a  complete  intrathoracic  lobe  going  out  from  the  left  lobe.  She 
subsequently  developed  a  goiter  on  the  thyroglossal  duct  just 
above  the  hyoid  bone.     This  also  was  removed. 

Aberrant  Goiters 

Owing  to  the  failure  of  the  thyroglossal  duct  to  become 
atrophic  or  to  the  displacement  of  thyrogenic  tissue,  it  is  pos- 
sible to  find  accessory  thyroids  anywhere  between  the  foramen 
cecum  and  the  normally  situated  thyroid  gland  and  even  as  low 
as   the   aortic   arch.     A  diagram   from  v.   Enselsberg's  book 


Fig.  67. — Diagram  showing  the  possibilities  in  aberrant  goiters.  A,  the  normally  situated 
gland;  B,  intrathoracic  lobe;  C,  detached  lobe  near  the  angle  of  the  jaw;  D,  sublingual  lobe; 
E,  lobe  near  the  angle  of  the  jaw  but  attached  to  the  upper  pole  by  a  fibrous  band;  F,  pre- 
tracheal lobe    (which  is   most  often  cystic) ;    G,  thyroglossal  duct. 

helps  to  visualize  the  usual  distribution  of  aberrant  goiters 
(Fig.  67). 

Accessory  thyroid  glands  are  most  common  in  the  lateral 
regions  of  the  neck.  These  evidently  are  displacements  from 
the  normally  situated  lateral  anlages  for  in  many  instances  they 
retain  fibrous  attachments  to  the  lateral  lobes.  However,  in  a 
case  reported  by  Eeynier  (Bull,  et  mem.  de  la  Soc  de  Chir.,  1906, 
xxxii,  901)  a  laterally  situated  cystic  thyroid  seemed  to  have 
attachment  to  the  thyroglossal  duct.    Thyroid  tissue  alleged  to 


150  DISEASES    OF    THE    THYROID   GLAND 

have  been  found  in  remote  parts  of  the  body  must  be  ascribed 
to  other  influences. 

Lingual  Goiter. — Tliyroid  nodules  at  the  base  of  the  tongue 
are  among  the  rarer  anomalies  of  displacement.  About  50  cases 
have  been  recorded  in  the  literature  according  to  Jorge  and 
Layern  (Kev.  de  la  Asoc,  Buenos  Aires,  August,  1918,  Vol.  29). 
These  figures  give  an  erroneous  idea  of  the  frequency  of  its  oc- 
currence. I  find  on  inquiry  that  most  surgeons  of  considerable 
experience  have  seen  one  or  more.  In  two  instances  it  appears 
that  the  lingual  was  the  only  thyroid  tissue  the  individual 
possessed.  In  order  to  avoid  depriving  the  patient  of  the  only 
thyroid  tissue  she  possessed,  it  would  be  advisable  to  make  an 
incision  at_the  site  of  the  normal  thyroid  and  demonstrate 
its  presence,  or  absence.  Myxedema  followed  the  removal  of  a 
large  lingual  goiter  in  Seldowitch's  case.  On  the  contrary  the 
patient  may  be  unduly  well  provided.  I  once  removed  a  very 
large  colloid  goiter  from  a  patient  who  had  a  lingual  goiter  the 
size  of  a  hulled  walnut.  The  lingual  goiter  gave  her  no  trouble 
and  she  preferred  to  keep  it.  After  the  removal  of  the  normally 
situated  goiter  the  lingual  one  shrank  and  has  given  her  no 
trouble,  noAv  ten  years  since  the  operation.  This  anomaly  is 
present  more  often  in  women  than  in  men,  in  the  proportion  of 
6 :1.  It  has  been  observed  in  all  ages  from  birth  to  seventy-seven 
years,  but  is  most  common  between  the  ages  of  fifteen  and  forty. 

Symptoms. — Lingual  goiters  develop  gradually  and  exer- 
cise an  unfavorable  influence  only  by  interfering  T\dth  the  func- 
tion of  deglutition  and  speech.  AATien  the  growth  is  rapid  or 
when  some  accident  befalls  it,  such  as  acute  inflammation  or 
hemorrhage  into  its  substance,  respiration  may  be  seriously 
interfered  with.  In  some  instances  thyrotoxic  symptoms  have 
attended  the  enlargement  of  lingual  goiters.  They  vary  in  size 
from  a  small  marble  to  that  of  a  walnut  or  even  a  hen's  egg. 
"When  large,  they  may  be  palpated  in  the  liyoid  region  (Ber- 
ger.  Bull,  et  mem.  Soc  de  Chir.,  1906,  xxxii,  1161).  They  are 
rounded  or  somewhat  lobulated,  the  mucous  membrane  covering 
them  contains  large  veins.  The  tumor  is  elastic,  but  not  fluctu- 
ating unless  secondary  changes  have  taken  place.  They  are  situ- 
ated at  the  base  of  the  tongue  and  may  project  upward  so  that 
they  are  plainly  visible,  but  sometimes  they  are  deeply  situated 


GOITERS   IX    UXUSUAL   PLACES  151 

SO  that  especial  effort  is  required  to  see  them  and  if  small,  a 
laryngeal  mirror  mnst  be  emploj'ed. 

DiAGXOsis. — Dermoids  at  the  base  of  the  tongue  are  most 
apt  to  be  mistaken  for  lingual  goiters.  The  dermoids  grow  more 
rapidly,  fluctuate  or  pit  on  pressure  and  the  covering  mucosa 
is  not  vascular  and  the  color  is  whitish  or  yellow.  Cysts  in  this 
region  are  situated  usually  in  the  midline,  the  surface  is  bluish, 
sometimes  translucent,  and  they  are  tense,  elastic,  or  fluctuat- 
ing. Gummas  are  deeply  imbedded  in  the  substance  of  the 
tongue  and  the  duration  is  not  so  long  as  in  lingual  thyroids. 
Tuberculomas  are  fungoid,  and  lung  involvement  can  be  demon- 
strated in  most  instances. 

Treatment. — Excision  is  the  best  treatment.  Because  of 
the  great  tendency  to  bleed,  a  preliminary  tracheotomy  is  per- 
formed as  done  by  some  surgeons  (Sterling,  Ann.  Surg,,  1907, 
xlvi,  826)  or  the  anesthesia  is  given  by  intratracheal  insuffla- 
tion. Berger  operated  on  his  patient  under  chloroform  anes- 
thesia, but  had  much  trouble  with  hemorrhage  and  cyanosis. 
Mass  ligation  about  the  tumor  controls  hemorrhage.  Harsha 
(Surg.  Clinics  of  Chicago,  1918,  ii,  312)  and  Berger  made  an  in- 
cision under  the  jaw  and  drew  the  tongue  do^^^l  through  the 
incision.  This  made  the  tumor  readily  accessible.  This  seems 
to  me  to  be  the  safest  procedure. 

Aberrant  Tumors  of  the  Submaxillary  Region. — These  are 
the  most  common  of  the  aberrant  tumors.  They  are  usually 
found  most  frequently  in  the  midperiod  of  life.  I  have  seen  none 
before  twenty-five  or  after  fifty-five.  All  that  I  have  seen  have 
been  in  women. 

Symptoms. — They  appear  as  ovoid  tumors  between  the  an- 
terior border  of  the  sternomastoid  and  the  border  of  the  lower 
jaw  (Fig.  68).  They  vary  in  size  from  that  of  a  bean  to  that 
of  an  orange.  They  cause  no  disturbance  except  from  their  size 
and  the  disturbance  is  cosmetic  rather  than  physical.  Thej^  are 
well  encapsulated  and  move  freely  in  all  directions  and  are  quite 
painless  on  pressure. 

DiAGxosis. — Aberrant  goiters  in  this  situation  must  be  dif- 
ferentiated from  a  great  variety  of  tumors.  Their  long  history 
differentiates  them  from  malignant  growths  and  their  great  mo- 
bility distinguishes  them  from  most  other  tumors  in  this  region. 


152 


DISEASES    OF    THE    THYKOID   GLAND 


Carotid  tumors  are  not  movable  in  a  vertical  direction.  Thyro- 
g'lossal  cysts  are  more  elastic  and  usually  can  be  made  to  bulge 
into  the  floor  of  the  mouth  when  pressed  upon.  They  are  differ- 
entiated from  mixed  tumors  of  the  submaxillary  gland  by  the 
fact  that  the  latter  are  firmer  than  goiters.  AVhen  the  aberrant 
lobe  is  attached  to  the  upper  pole  of  the  normally  situated 
goiter,  a  tugging  on  the  aberrant  lobe  can  be  felt  during  degluti- 
tion.    If  the  diagnosis  is  not  made  before  operation,  they  are 


Fig.   68. — An   aberrant   goiter   near   the  angle   of   the  jaw.     This   lobe   was   the    sole   cause   of   a 

thyrotoxicosis. 


differentiated  from  carotid  tumors  by  the  fact  that  they  are  not 
associated  with  the  carotid  vessels. 

Treatment. — They  are  more  easily  removed  than  any  other 
tumor  of  the  neck.  They  have  no  attachment  and  but  little 
blood  supply. 

Intratracheal  Struma. — Thyroid  tissue  within  the  trachea 
has  been  described  in  some  16  cases.  Whether  these  shall  be 
regarded  as  embryonal  displacements  or  secondary  growth  into 
the  trachea  from  a  normally  situated  gland  has  not  yet  been 


GOITERS    IN    UNUSUAL   PLACES  153 

detennined.  They  liave  been  noted  all  the  way  from  beneath 
the  vocal  cords  (Paltoni')  to  the  tracheal  bifurcation  (Radistock, 
Beitr.  z.  jDath.  Anat.,  1888,  iii,  288).  The  majority  have  been 
noted  about  the  level  of  the  first  tracheal  ring.  The  usual  situ- 
ation relative  to  the  circumference  of  the  trachea  has  been  in 
the  posterior  or  lateral  wall  or  the  posterolateral.  Paltouf 
(Beitr.  z.  path.  Anat.,  1892,  ii,  71)  Avas  able  to  trace  a  direct 
connection  between  the  intratracheal  and  the  normally  situated 
gland,  and  he  reasons  from  this  that  there  must  be  a  like  con- 
nection in  the  other  cases.  As  Grunenwald  (Beitr.  z.  klin.  Chir., 
1905,  xlv,  711)  points  out,  such  a  connection  would  be  hard  to 
hypothecate  for  the  tumors  located  in  the  posterior  wall  of  the 
tracliea,  and  even  more  difficult  of  explanation  is  Rodestrak's 
case  in  which  the  tumor  was  situated  at  the  tracheal  bifurca- 
tion. All  things  .considered,  it  seems  safe  to  classify  these  intra- 
tracheal masses  along  with  the  aberrant  thyroids. 

Symptoms. — As  might  be  anticipated,  women  are  more  com- 
monly affected  than  men.  The  proportion  of  1 :4  is  given.  They 
are  most  frequently  noted  in  early  adult  life.  The  reported 
cases  range  in  age  from  twelve  to  thirty-four  years,  though  my 
patient  was  fifty-eight  years  old.  Most  generally  there  is  a  pro- 
dromal difficulty  of  respiration,  for  months  or  years  Avitli  a  more 
or  less  sudden  onset  of  threatening  dyspnea  which  in  Paltouf 's 
case  required  an  emergency  tracheotomy.  In  Rodestock's  case  a 
bronchiectasis  with  suppuration  developed  following  the  drain- 
age, of  which  the  patient  died.  The  tumor  was  found  at  the  bi- 
furcation. Six  of  the  reported  cases  were  located  on  the  poste- 
rior wall,  six  on  or  near  both  sides,  two  exclusively  on  one  side 
and  one  was  attached  to  the  anterior  wall.  In  my  case  the  base 
of  attachment  was  to  the  lateral  wall  (Fig.  69).  The  thyroid 
lobe  had  previously  been  removed  for  malignancy  and  no  at- 
tachment to  the  trachea  at  this  point  was  noted. 

Diagnosis. — In  most  of  the  cases  a  rounded  tumor  mass 
covered  with  normal  mucosa  has  been  observed  with  the  laryn- 
goscope. AVhen  deeply  lying  they  may  escape  observation,  or  in 
very  dyspneic  patients  satisfactory  obsei'vation  may  not  be  pos- 
sible. In  my  patient  (Hertzler:  Clinical  Surgery  by  Case  His- 
tories; Mosby,  St.  Louis,  i,  j).  205)  a  corpulent  woman  of  fifty- 
eight,  it  was  not  possible  to  see  below  the  vocal  cords.    Two  of 


154 


DISEASES    OF    THE    THYROID   GLAND 


the  cases  reported  ^vere  autopsy  findings.  These  tumors  are 
often  associated  Avith  normal  thyroids  though  in  several  there 
was  a  moderate  struma  and  in  my  case  the  patient  had  already 
been  operated  twice  for  thyroid  enlargement.  Usually  there  is 
a  history  of  gradual  onset. 

Paltouf 's  case    was  mistaken  for  a  s}T)hilitic  and  Rode- 
stock's  for  a  tuberculous  perichondritis.     This  error  is  more 


Fig.    69. — Intratracheal   goiter.     A,    as   it   appeared   at   operation;    B,    diagrammatic    presentation 
of   a   cross   section,   showing   the   lateral   attachment  of  its   base. 

likely  to  be  made  when  the  tumor  is  situated  just  below  the  vocal 
cords  than  when  it  is  located  more  deeply.  In  my  patient  the 
tumor  was  4  or  5  cm.  below^  the  cords  and  its  nature  could  be 
easily  determined. 

Intratracheal  strumas  must  be  differentiated  from  a  number 
of  equally  rare  conditions.    Fibromas  are  lighter  in  color  and 


GOITERS    IX    UNUSUAL   PLACES  155 

are  pedunculated,  while  strumas  are  attach-ed  by  a  broad  base 
and  are  red  in  color.  Papillomas  have  a  distinctive  surface 
characterizing  these  tumors  elsewhere.  Chondromas  are  firm 
and  lighter  in  color.  Still  more  rare  tumors  are  lymphomas 
and  lipomas.  Inspection  does  not  make  it  possible  to  make  the 
differentiation.  Syphilis  is  usually  attended  by  symptoms  else- 
where in  the  body.  In  case  of  doubt  the  therapeutic  test  may  be 
applied.  It  must  be  remembered  that  thyroid  tissue  may 
respond  to  iodine  therapy.  In  Neumeyer's  cases  (Monatsch.  f. 
Ohrenh.,  1904,  xxxviii,  388)  the  tumor  rapidly  shrank  under 
iodine  treatment.  A  goiter  in  the  normal  situation  also  lessened. 
Neumeyer  argued  because  of  this  that  the  intratracheal  tumor 
likewise  must  have  been  thyrogenic. 

Treatment. — My  patient  was  treated  by  performing  a 
tracheotomy  and  excising  the  tumor  with  a  thermocautery  and 
the  trachea  closed.  No  difficulty  followed.  Griinwald's  case 
was  treated  by  excision  witli  ligation  of  bleeding  points.  A 
granuloma  sprang  up  requiring  a  secondary  ligation.  Two  of 
the  cases  were  treated  by  partial  destruction,  both  resulting  in 
failure  to  cure.  Paltouf 's  case  was  treated  by  compression.  In- 
fection and  acute  thyroiditis  followed  and  despite  drainage  the 
patient  died.  Freer  (Jour.  Am.  Med.  Assn.,  1901)  punctured 
a  tumor  with  an  electrocautery.  Swelling  followed,  necessi- 
tating a  tracheotomy.  In  two  cases  ( Neumeyer 's)  iodine  and 
thyroid  extract  were  given  with  good  results.  This  treatment 
would  be  permissible  when  the  diagnosis  is  made  early  before 
threatening  dyspnea  has  developed,  a  desideratum  only  rarely 
met.  On  the  whole,  laryngofissure  with  excision  with  the  electric 
cautery  as  practiced  in  my  case  seems  to  be  the  most  rational 
treatment. 


CHAPTER  VII 

HOSPITAL  MANAGEMENT  OF  GOITER  PATIENTS 

By  Dr.  Victor  E.  Chesky 

The  hospital  management  of  tlie  patient  includes  the  care 
from  the  time  she  enters  the  hospital  until  dismissal.  It  in- 
cludes the  preoperative  treatment,  both  of  the  goiter  itself  and 
associated  diseases,  the  postoperative  treatment  and  the  treat- 
ment of  any  complications  that  may  arise. 

PREOPERATIVE  TREATMENT 

The  preoperative  treatment  of  the  nontoxic  and  the  toxic 
goiter  is  essentially  different. 

Nontoxic  Goiter 

The  preoperative  treatment  of  the  nontoxic  goiter  patient 
is  that  accorded  any  ordinary  surgical  patient  that  comes  in  for 
operation.  The  history  and  physical  examination  are  made  with 
the  view  of  discovering  any  contraindications  for  operation  or 
any  factor  that  may  complicate  it.  The  region  of  the  goiter  is 
x-rayed  to  discover  whether  there  are  any  substernal  prolonga- 
tions, or  any  deviations  of  the  trachea  from  its  normal  site.  The 
vocal  cords  are  examined  to  note  the  presence  of  a  preoperative 
paralysis.  If  there  is  a  myocardial  disturbance,  rest  and  heart 
tonics  are  given. 

Toxic  Goiters 

With  the  thyrotoxic  cases  much  more  careful  and  elaborate 
preparation  is  necessary.  Each  patient  must  be  managed  ac- 
cording to  her  needs. 

Preliminary  Examination. — ^AV^hen  the  thyrotoxic  patient  en- 
ters the  hospital,  if  the  toxicity  is  at  all  pronounced,  she  is  told 
she  will  be  placed  under  observation  for  a  short  time  before  the 
date  of  the  operation  can  be  determined.    During  this  period  the 

156 


HOSPITAL    MAXAGE.MEXT    OF   GOITER    PATIENTS  157 

extent  of  toxicity  is  determined  as  nearly  as  possible.  From  the 
history  it  can  be  learned  in  a  general  way  wliether  the  patient 
is  on  the  downward  curve  headed  toward  a  toxic  crisis,  whether 
her  symptoms  are  spontaneously  subsiding  or  whether  they 
liave  reached  a  stationary  plane.  The  history  shows  the  length 
of  time  the  toxemia  has  existed,  the  number,  and  to  some  extent 
the  severity,  of  the  toxic  crises  she  has  passed  through.  The 
patient's  variations  in  weight  are  carefully  gone  into,  her 
normal  weight,  her  estimate  of  her  present  weight  and  she  is 
then  Aveighed  to  test  the  accuracy  of  her  judgment.  The  ex- 
tent of  damage  done  the  parenchymatous  organs  by  previous 
crises  is  determined  by  a  general  physical  examination.  The 
toxic  status  having  been  determined,  the  preparation  for  opera- 
tion is  begun. 

Rest. — Rest,  as  complete  as  is  possible  to  obtain,  is  by  far 
the  most  important  part  of  the  preoperative  treatment.  By  rest 
both  mental  and  i^hysical  rest  is  implied;  the  former  being  much 
more  difficult  to  obtain.  Apprehension,  distrust,  and  worry  over 
domestic  or  financial  affairs  are  only  a  few  of  the  conditions  of 
mind  encountered  in  thyrotoxic  cases.  Sometimes  patients  en- 
ter only  at  the  insistence  of  relatives  thus  adding  another 
element  to  the  obstacle  in  the  way  of  securing  mental  repose. 
One  should  always  remember  that  he  is  dealing  not  alone  with  a 
physical  condition  but  also  with  a  type  of  neurosis  which  at 
times  amounts  to  a  mild  mania. 

Kindness  and  patience  on  the  part  of  doctor  and  nurses  will 
go  a  long  way  toward  allaying  mental  unrest.  Kindness  on  the 
part  of  the  surgeon  should,  however,  be  backed  up  by  an  un- 
obtrusive firmness  which  makes  the  patient  realize  that  he  ex- 
pects to  have  his  instructions  carried  out.  Correction  of  the  pa- 
tient by  doctors  or  nurses  should  never  amount  to  scolding  or 
abuse.  One  should  always  remember  the  high  nervous  tension 
of  the  patient.  Crotti  puts  it  admirably  when  he  says  ' '  It  must 
never  be  forgotten  that  thyrotoxic  patients  are  highly  sensitive 
and  often  react  with  a  veritable  thyrotoxic  explosion  to  some 
trivial  annoyance. ' '  It  has  been  a  common  observation  with  us 
to  have  patients  come  in  looking  the  picture  of  an  extreme  thy- 
roid intoxication  who  after  a  few  hours'  rest  during  which  they 
are  kindly  treated  by  their  nurses  and  receive  the  assurance 


158  DISEASES    OF    THE    THYROID   GLAXD 

from  their  doctor  that  all  will  be  well,  lose  their  initial  hospital 
fear  and  present  an  entirely  different  ai^pearance. 

The  patient  should  be  placed  in  a  comfortable  room  and 
things  arranged  as  far  as  possible  to  her  liking.  Quiet  should 
prevail  both  within  the  room  and  in  proximity  to  it.  Loquacious 
relatives  and  friends  should  be  excluded.  A  few  chosen  rel- 
atives or  friends  may  be  allowed  to  visit,  for  they  can  often  aid 
materially  in  malting  the  patient  satisfied  with  her  enforced  rest 
and  help  alla,y  her  apprehension  for  the  coming  operation.  The 
duration  of  their  visits  should  stop  short  of  exhausting  the  pa- 
tient. Toxic  patients  do  not  need  entertainment  and  very  little 
reading  should  be  indulged  in  by  them. 

The  patient  should  be  in  bed  most  of  the  time  and  the  se- 
vere cases  should  not  be  allowed  to  leave  the  bed  at  all.  No 
hard  and  fast  rules  can  be  made,  however,  in  regard  to  rest  in 
bed.  One  must  study  the  type  of  patient.  Some  are  satisfied  to 
lie  in  bed  and  do  better  on  a  back  rest  elevated  from  30  to  45 
degrees  for  several  hours  during  the  day  w^hile  others  are 
allowed  a  chair  for  two  or  three  hours  at  a  time  to  take  the  edge 
off  their  nervousness.  Every  patient  should  be  cautioned 
against  making  any  sudden  physical  movements  such  as  spring- 
ing from  a  reclining  to  a  sitting  posture,  a  type  of  calisthenics  I 
have  frequently  seen  indulged  in  by  these  patients. 

By  tact  and  care  most  patients  can  be  made  to  take  the  re- 
quired amount  of  rest.  There  are  a  few  who  are,  because  of  ex- 
cessive nervousness,  entirely  beyond  the  surgeon's  control. 
They  continually  chafe  under  the  restraint  and  after  weeks  of 
rest  in  the  hospital  are  no  better,  or  are  even  worse,  than  at  the 
time  of  entrance.  Some  of  the  severe,  acute  intoxications  re- 
spond to  no  treatment  and  rapidly  progress  to  a  fatal  termina- 
tion. 

Diet. — A  toxic  goiter  patient  must  have  the  greatest  amount 
of  food  possible  to  counteract  the  excessive  oxidation  the  disease 
causes.  This  increase  in  katabolism  is  shown  by  the  basal  met- 
abolic test  and  the  metabolic  rate  is  a  fairly  true  index  of  the  ex- 
tent of  the  toxemia.  It  is  estimated  that  a  severely  toxic  patient 
at  rest  in  bed  requires  as  much  food  as  a  man  at  hard  manual 
labor,  that  is  3,500  to  4,000  calories  per  day. 

These  patients  do  better  on  a  preponderatingly  carbohy- 


HOSPITAL   MANAGEMENT   OF  GOITER   PATIENTS  159 

drate  diet.  If  the  diet  is  largely  protein  tliey  are  apt  to  lose 
their  appetite.  The  food  must  not  be  of  the  heavy  indigestible 
.  character,  with  a  large  amount  of  residue,  if  we  are  to  get  the 
patient  to  take  the  requisite  number  of  calories. 

If  the  patient  does  not  take  enough  food  at  mealtime,  drinks 
of  lemonade  containing  50  gin.  of  lactose  to  the  glassful  may  be 
given  between  meals.  This  gives  the  patient  200  calories  per 
glass  and  the  amount  of  sugar  does  not  make  the  drink  nauseat- 
ingly  sweet.  In  some  cases  60  gin.  or  240  calories  may  be  given. 
It  may  also  be  given  occasionally  in  hot  peppermint  water. 

Fortunately  the  patients  usually  have  a  good  appetite, 
sometimes  a  ravenous  one,  which  aids  materially  in  solving  the 
feeding  problem.  Feeding  should  be  continued  day  and  night 
up  to  the  time  of  operation  together  with  the  forced  giving  of 
liquids  and  especially  the  lactose  drinks.  This  is  the  surest  pro- 
I)liylactic  treatment  of  postoperative  acidosis. 

Drugs. — No  attempt  will  be  made  to  discuss  the  various 
drugs  used  in  the  medical  treatment  of  goiter  but  only  those 
which  are  useful  after  operative  procedure  has  been  determined 
upon. 

The  principal  drugs  used  are  the  sedatives  which  insure  the 
patient  rest  and  sleep. 

Sodium  bromide,  gr.  xv  to  gr.  xx  three  times  daily,  or  in 
some  patients  a  singie  large  dose  as  gr.  xxx  to  xl  once  daily  is 
about  the  required  amount  to  take  the  edge  off  the  patient's 
nervousness  and  to  secure  sleep. 

If  the  patient  sleeps  poorly  despite  the  above  treatment 
several  gr.  x  doses  of  veronal  or  sodium  bromide  gr.  xx  with 
chloral  hydrate  gr.  x  given  in  a  glass  of  hot  water  or  hot  milk 
an  hour  before  bedtime  will  usually  correct  the  insomnia.  In 
some  extremely  nervous  cases,  who  do  not  react  well  to  these 
drugs,  codeine  gr.  ss  to  gr.  1  hypodermically  often  acts  very 
well. 

About  one  hour  before  operation  the  patient  should  receive 
morphine  sulphate  gr.  14  hypodermically  if  the  work  is  to  be 
done  under  a  local  anesthetic  as  is  the  practice  in  this  hospital; 
if  under  a  general  anesthetic  a  small  dose  as  gr.  %  to  %  will  in- 
sure the  patient's  taking  the  anesthetic  with  a  minimum  of  ex- 
citation. 


160  DISEASES    OF    THE    THYROID   GLAXD 

Vomiting  and  Diarrhea. — Some  of  the  cases  of  toxic  goiter 
at  one  time  or  aiiotlier  during  their  toxic  crises  suffer  from  a 
diarrhea.  Increased  metabolism  causes  an  excessive  secretory 
activity  of  both  the  stomach  and  intestines.  This  stimulates  the 
intestines  to  the  production  of  copious  watery,  grayish  appear- 
ing stools.  They  appear  to  be  devoid  of  bile  but  the  volume  of 
bile  is  not  decreased.  A  powder  consisting  of  a  half  grain  each 
of  calomel  and  opium  given  every  4  hours  will  often  check  the 
diarrhea  Avhile  in  some  cases  opium  and  belladonna  suppositories 
help  quiet  the  irritable  intestine. 

The  hyperchlorhydria  together  with  the  general  irritability 
and  spasticity  of  the  stomach  musculature  often  produces  per- 
sistent vomiting.  In  that  event  fluids  by  mouth  should  be  dis- 
continued allowing  only  a  little  cracked  ice.  Water  should  be 
given  by  proctoclysis.  Gastric  lavage  should  be  used  only  as  a 
last  resort. 

Management  of  Constipation. — Mild  laxatives  are  given  if 
necessary  during  the  period  of  preoperative  care,  and  a  soap 
suds  enema  is  given  the  night  before  operation.  Even  this  is 
unnecessary  if  the  bowels  move  well  with  laxatives.  It  is  im- 
portant that  the  patient  be  not  disturbed  by  an  enema  a  short 
time  before  operation. 

Time  of  Operation. — Thyrotoxic  patients  constantly  harass 
the  surgeon  with  questions  as  to  the  time  they  will  be  operated 
on.  As  a  rule  they  wish  to  get  it  over  with  regardless  of  their 
condition.  It  is  best  that  no  date  for  operation  be  set  as  many 
grow  more  nervous  as  the  time  approaches.  I  have  also  seen  a 
marked  increase  of  the  toxic  symptoms  follow  the  disappoint- 
ment incident  to  a  postponement  of  operation. 

The  patient  should  be  told  that  all  of  the  preparation  is  for 
the  purpose  of  making  operation  a  safe  procedure  and  that  no 
one  can  tell  the  length  of  the  preparation  necessary.  The  sur- 
geon should  never  set  a  limit  on  that  time  until  he  is  absolutely 
sure.  When  the  time  for  operation  has  been  determined  on,  the 
patient  is  told  the  time  in  a  simple,  confident  way.  The  per- 
sonality of  the  operator  and  the  consequent  confidence  he  can 
inspire  is  a  large  factor  in  securing  the  desired  tranquillity  on 
the  part  of  the  patient. 


HOSPITAL   MAXAGEMEXT   OF  GOITER   PATIEXTS  161 

POSTOPERATIVE  TREATMENT 

The  postoperative  treatment  of  goiter  varies  according  to 
tlie  type  of  goiter  for  which  the  patient  has  been  ojjerated  on.  In 
the  pnrely  nontoxic  type  the  treatment  resolves  itself  into  that 
accorded  any  clean  operative  Avound,  in  which  the  operation  is 
not  followed  by  any  marked  reaction  and  in  which  the  prob- 
ability of  complications  is  rather  remote. 

On  the  other  hand,  the  patient  suffering  from  the  exophthal- 
mic tj^pe  requires  a  great  deal  of  postoperative  care  because  the 
toxicity  is  increased  after  the  operation  and  the  tendency  to 
comi)lications  is  much  greater. 

The  purpose  of  this  section  is  to  discuss  the  treatment  of  the 
toxic  type  after  operation,  together  with  the  treatment  of  com- 
plications which  may  arise. 

General  Nursing  Care. — The  patient  should  be  under  the 
care  of  a  special  nurse,  preferably  one  who  has  been  with  the 
patient  a  day  before  the  operation.  This  allows  the  patient  to 
become  accustomed  to  the  nurse  and  permits  the  establishment 
of  confidence  on  the  part  of  the  patient  in  the  nurse.  This  aids 
materially  in  allaying  the  nervousness  incident  to  the  operation. 
The  nurse  should  be  quiet,  even-tempered,  and  able  to  control 
her  patient  without  friction. 

After  operation,  the  patient  should  be  placed  in  a  partly 
darkened,  cool  room  and  made  as  comfortable  as  possible.  Quiet 
should  be  maintained  both  within  the  room  and  in  the  proximity 
of  it.  Noise  that  the  ordinary  operative  patient  w^ould  not 
notice,  produces  a  marked  impression  on  a  patient  suffering 
from  a  thjToid  intoxication.  After  the  needs  of  the  patient  have 
been  attended  to  she  should  be  left  undisturbed.  Nothing  so 
irritates  a  highly  toxic  patient  as  a  nurse  who  thinks  that  she 
must  be  constantly  doing  something  in  order  to  best  serve  the 
interest  of  her  patient. 

Conversation,  reading,  or  any  other  form  of  entertainment 
is  not  only  unnecessary,  but  detrimental  at  this  time.  Relatives 
and  friends  should  be  excluded  from  the  room  until  the  post- 
operative toxicity  is  markedly  reduced. 

Vomiting. — Postoperative  vomiting  is  rarely  severe  except 
in  cases  of  acidosis.     Most  patients  operated  on  under  local 


162  DISEASES    OF    THE    THYROID   GLAND 

anesthesia  do  not  vomit  at  all,  while  a  few  do  vomit,  probably 
because  of  the  preoperative  dose  of  morphine.  Some  surgeons 
believe  that  novocaine  also  causes  nausea  and  it  is  true  we  occa- 
sionally see  instances  of  nausea  after  almost  any  type  of  opera- 
tion in  which  novocaine  is  used.  After  general  anesthesia  the 
vomiting  is  usually  more  severe. 

If  the  patient  vomits,  but  little  Avater  by  mouth  should  be 
given,  but  if  the  nausea  persists,  the  stomach  should  be  washed. 
If  the  vomiting  still  continues,  which  is  extremely  rare,  fluids 
should  be  withheld  by  mouth  and  water  given  by  proctoclysis, 
or  by  hypodermoch'Sis. 

Pain. — Severe  pain  does  not  usually  follow  thyroidectomy. 
Many  complain  of  only  a  rather  intense  soreness  on  swallowing. 
Occasionally  a  patient  complains  of  extremely  severe  pain  in  the 
wound  region  which  radiates  upward  toward  the  ears.  Such 
patients  should  have  opiates  for  their  relief.  Codeine  gr.  ss 
given  hypodermically  is  usually  sufficient,  but  when  the  pain  is 
especially  severe,  morphine  gr.  %  to  %  should  be  given. 

Restlessness  and  Nervousness. — These  symptoms  are  the 
measure  of  toxicity.  Their  severity  depends  on  the  extent  of 
the  thyroid  intoxication  which  existed  previous  to  operation. 
They  are  increased  by  the  operation  possibly,  as  many  surgeons 
believe,  by  the  increased  absorption  of  toxic  substances  from  the 
manipulation  of  the  thyroid  during  the  operation  or  from  the 
cut  surface  exposed  by  the  excision.  To  combat  the  toxemia  one 
keeps  the  patient  as  comfortable  as  possible  and  in  general  car- 
ries out  the  suggestions  given  under  the  heading  of  General 
Nursing  Care. 

Codeine  or  morphine  hypodermically  are  often  necessary. 
If  the  restlessness  is  not  accompanied  by  severe  pain,  codeine 
gr.  ss  is  usually  sufficient  but  when  it  is  severe  or  extreme  rest- 
lessness develops,  morphine  gives  better  results. 

I  have  not  found  other  sedatives  very  efficient  in  these 
cases.  The  large  doses  necessary  to  get  results,  the  slowness  of 
their  action,  and  their  depressing  after-effects  make  them  ob- 
jectionable. These  patients  are  also  sometimes  nauseated  and 
any  medicine  by  mouth  increases  the  disturbance. 

Control  of  Temperature. — Toxic  goiters  almost  without  ex- 
ception have  a  fever  after  operation.    The  height  of  the  tern- 


HOSPITAL   IVIAXAGEMEXT   OF  GOITER   PATIENTS  163 

perature  seems  to  be  in  direct  proportion  to  the  toxicity  of  the 
goiter.  The  temperature  often  goes  to  102°  or  to  103°  and  may 
go  even  higher.  The  patient  becomes  very  restless  and  seems 
fairly  to  radiate  heat.  Reducing  the  temperature  helps  allay 
the  restlessness  and  so  conserves  the  patient's  strength. 

The  temperature  is  best  controlled  by  placing  an  ice  bag 
on  her  head  or  the  whole  body  may  be  sponged  with  cool  water, 
or  a  number  of  ice  bags  may  be  placed  about  the  patient.  The 
patient  should  be  under  constant  observation,  and  if  any  cyan- 
osis develops,  the  ice  bags  should  be  immediately  removed. 

Treatment  of  Toxemia. — Toxic  goiters  soon  after  operation 
pass  through  a  period  during  which  there  is  a  marked  exacer- 
bation of  their  toxic  symptoms.  This  is  noticed  within  a  few 
hours.  By  36  to  48  hours  the  toxic  symptoms  are  at  their 
height  and  soon  begin  to  subside.  The  prognosis  is  grave  if 
the  symptoms  continue  beyond  this  time. 

The  patient  at  the  height  of  her  toxemia  tosses  about  the 
bed;  the  eyes  are  open  wide,  even  the  exophthalmos  seeming 
to  be  increased;  the  skin  is  flushed  and  feels  hot  to  the  touch; 
the  arms  and  legs  are  in  almost  constant  motion  and  sometimes 
there  is  a  delirium  during  Avhich  the  patient  mutters  and  talks 
incessantly.  The  pulse  is  rapid,  sometimes  irregular,  and  the 
respiratory  rate  is  increased. 

The  treatment  of  the  toxemia  consists  of  increasing  the 
elimination  by  the  giving  of  large  quantities  of  fluids.  Often 
these  are  w^ell  taken  by  mouth,  but  the  total  intake  may  be  in- 
creased by  giving  fluids  by  proctoclysis.  An  almost  continuous 
proctoclysis  may  be  given,  stopping  for  a  few  hours  if  the  pa- 
tient begins  to  expel  it.  Water  may  also  be  given  subcutane- 
ously  and  this  should  be  done  if  not  enough  fluid  can  be  given 
by  the  other  avenues.  The  only  objection  to  this  method  is  the 
amount  of  disturbance  which  it  sometimes  causes.  A  prelim- 
inary hypodermic  of  morphine  often  quiets  the  patient  enough 
to  overcome  this  objection.  The  giving  of  lemonade  sweetened 
with  lactose  often  is  much  appreciated  immediately  after  opera- 
tion and  serves  the  double  purpose  of  giving  fluids  and  also 
also  an  easily  assimilated  carbohydrate  to  burn. 

Tracheitis  and  Laryngitis. — Trauma  in  such  close  proximity 
to  the  trachea  almost  always  produces  some  reaction  within  it. 


164  DISEASES    or    THE    THYROID   GLAXD 

The  more  closely  and  extensively  the  goiter  is  adherent  to  the 
trachea,  the  greater  will  be  this  reaction.  This  manifests  itself 
in  an  accumulation  of  viscid  mucus  in  the  trachea  and  larynx. 
It  makes  breathing  difficult,  annoys  the  patient,  and  increases 
the  nervousness.  Much  can  be  done  at  the  operation  to  lessen 
this  complication  by  leaving  the  tissue  intact  immediately  sur- 
rounding the  trachea. 

Drinks  of  lemonade,  orangeade  or  of  water  will  relieve  the 
pharynx  and  steam  inhalations  with  compound  tincture  of  ben- 
zoin added  lessens  the  viscidity  of  the  mucus  and  renders  its 
expulsion  less  difficult. 

Care  of  the  Wound. — The  care  of  the  wound  following  a 
thyroidectomy  is  in  general  that  accorded  any  other  clean  oper- 
ative wound.  If  the  wound  is  closed  without  drainage,  as  is  the 
practice  in  this  hospital,  the  dressings  should  be  left  undis- 
turbed until  the  fourth  day  unless  some  complication  arises. 

In  most  cases  there  is  a  little  oozing  of  blood  through  the 
line  of  incision  immediately  after  operation  which  causes  the 
gauze  dressing  to  adhere  to  it.  Because  of  this  every  subsequent 
turn  of  the  patient's  head  exerts  a  little  pull  on  the  incision  or 
sutures,  which  is  annoying  to  her.  If  the  dressing  is  raised  and 
this  piece  of  bloodsoaked  gauze  is  gently  separated  and  removed 
and  clean  gauze  is  allowed  to  come  into  contact  with  the  wound 
she  is  much  relieved.  This  appears  to  be  a  small  matter  to  con- 
sider, but  it  is  always  appreciated  by  the  hypersensitive  patient. 

After  about  four  days  the  skin  is  completely  healed  and 
the  sutures  are  removed.  The  early  removal  of  the  sutures  pre- 
cludes the  possibility  of  puncture  scars  where  the  sutures  pass 
through  the  skin. 

If  the  wound  has  been  drained,  the  drains  are  removed 
twenty-four  to  forty-eight  hours  after  operation.  If  the 
tissue  removed  is  large  in  amount  and  the  drainage  correspond- 
ingly greater,  the  drain  may  be  left  in  several  days  longer. 

In  the  wound  that  is  not  drained,  there  is  sometimes  seen  a 
marked  edema  of  the  tissues  both  above  and  below  the  incision. 
This  does  not  cause  much  pain  and  usually  subsides  in  about 
two  or  three  days.  If  the  swelling  is  excessive,  so  that  the  pa- 
tient complains  of  pain  or  of  a  feeling  of  pressure  on  the  trachea, 
several  layers  of  gauze  soaked  in  equal  parts  of  glycerine  and 


HospiTxiL  maxage:nlext  of  goiter  patiexts  165 

alcohol  and  applied  to  the  swollen  area  for  ten  to  twelve  hours 
will  cause  a  marked  reduction  of  the  swelling. 

From  about  the  fourth  to  the  seventh  day,  small  blebs,  due 
to  the  iodine  used  for  sterilizing  the  skin,  may  appear  in  the 
skin  in  the  line  of  incision,  which  contain  an  almost  clear  or 
brownish  serum.  If  not  treated,  they  finally  rupture  and  drain 
out.  As  soon  as  they  are  discovered  they  should  be  pricked  open 
with  a  sharp-pointed,  narrow-bladed  knife  and  the  fluid  ex- 
pressed. They  have  a  tendency  to  close  and  refill  and  should  be 
opened  daily  until  they  disappear. 

Sometimes  there  is  an  accumulation  of  fluid  in  the  wound. 
This  is  partly  from  the  cut  surface  of  the  gland  and  partly  from 
capillary  oozing.  It  often  gives  no  visible  evidence  of  its  pres- 
ence even  for  as  long  as  a  week  after  operation.  If  a  portion 
of  the  incision  remains  indurated  and  tender  to  slight  pressure, 
its  presence  should  be  suspected  and  the  patient  not  discharged 
from  the  hospital  until  its  ultimate  fate  is  determined.  The  in- 
durated area  will  often  fluctuate  as  late  as  two  weeks  after  op- 
eration and  finally  open  spontaneously  and  the  fluid  drain  out. 
If  this  occurs  after  the  patient  has  gone  home,  it  causes  con- 
siderable anxiety  to  the  patient  and  annoyance  to  the  surgeon. 
As  soon  as  any  fluctuation  is  noticed,  a  very  small  opening  made 
in  the  line  of  incision  will  allow  this  to  drain  out.  A  large  open- 
ing is  not  necessary  because  the  exudate  is  sterile. 

Treatment  of  the  Heart. — Patients  who  had  cardiopathies 
before  operation  may  require  continuation  of  treatment  after 
operation.  Myocardial  degeneration  may  result  from  a  long 
period  of  thyroid  intoxication,  or  from  a  goiter  which  has  ex- 
isted for  twenty-five  or  thirty  years  and  with  toxic  sj'mptoms  of 
recent  origin.  Whatever  be  the  cause  of  the  cardiac  disturb- 
ance, these  patients  should  be  kept  in  bed  and  given  digitalis  in 
some  form  until  compensation  is  restored. 

In  those  patients  with  a  damaged  heart  muscle  and  without 
signs  of  heart  failure  but  where  a  severe  toxic  reaction  after 
operation  is  anticipated,  digitalis  should  be  given  for  a  few  days 
before  operation  and  kept  up  until  the  toxemia  has  subsided. 
When  nausea  continues  some  days  after  operation,  digitalis  in 
the  form  of  tincture,  using  from  four  to  six  mils  may  be  placed 
in  a  pint  of  normal  solution  and  given  by  the  Murphy  drip. 


166  DISEASES    OF    THE    THYROID   GLAND 

Some  suitable  form  of  digitalis  may  also  be  given  liypodermi- 
cally  in  cases  where  urgency  exists  or  where  the  gastric  condi- 
tion contraindicates  its  being  given  by  mouth.  Morphine  or 
codeine  to  quiet  the  restlessness  does  much  to  save  the  heart. 
Ice  caps  over  the  cardiac  area  are  indicated  when  the  heart  rate 
is  extremely  rapid. 

Diet. — Feeding  should  be  begun  immediately  after  opera- 
tion; nourishing  drinks,  lactose  lemonade,  50  gm.  to  the  glass, 
and  soups  which  have  milk  as  the  vehicle  and  have  a  real  caloric 
value  should  be  the  first  nourishment.  Hospital  customs  die  a 
lingering  death  and  if  one  does  not  specify  the  fluids  to  be  given, 
surgeons  are  likely  to  find  their  patients  getting  that  ancient 
fraud,  broth,  which  consists  of  water  w^ith  a  trace  of  albumin  in 
the  form  of  extractives.  Lactose  may  be  used  as  the  sweetening 
in  any  liquid,  thus  greatly  increasing  its  nutritive  value.  Glu- 
cose may  also  be  given  in  the  proctoclysis. 

The  day  after  operation  the  patient  may  be  given  soft, 
easily  digested  foods,  and  the  diet  steadily  increased  from  this 
time.  The  food  should  be  largely  carbohydrates  without  much 
cellulose  residue  but  protein  and  fats  in  the  form  of  milk  and 
dairy  products  should  be  given.  Meat  should  not  be  given  until 
the  patient  is  entirely  recovered  from  the  operation  and  then 
only  fish  or  white  meat  and  these  very  sparingly. 

POSTOPERATIVE  COMPLICATIONS 

Since  the  principles  of  the  operative  technic  have  become 
common  knowledge,  there  are  few  operations  so  little  liable  to 
complications  as  are  the  operations  on  the  thyroid  gland.  Pneu- 
monia has  all  but  disappeared  with  general  anesthesia;  tetany 
with  the  preservation  of  the  parathyroids;  myxedema  with  the 
proper  preservation  of  sufficient  functioning  gland  and  vocal 
cord  paralysis  since  resection  has  supplanted  lobectomy.  How- 
ever, notwithstanding  the  greatest  technical  care,  complications 
still  appear  at  times.  These  will  be  discussed  in  the  following 
paragraphs. 

Collapse  of  the  Trachea 

Collapse  of  the  trachea  is  extremely  rare,  but  if  it  occurs  at 
all,  it  is  one  of  the  earliest  complications,  occurring  either  during 


HOSPITAL   MANAGEMENT   OF  GOITER   PATIENTS  167 

the  operation  or  immediately  following  it.  It  occurs  in  those 
cases  in  which  the  trachea  has  been  subjected  to  pressure  by  a 
hard,  or  usually  a  large  goiter  for  such  a  period  of  time  that  the 
cartilages  are  eroded.  During  the  operation,  collapse  usually 
occurs  when  a  partially  resected  thyroid  is  rotated  subjecting 
the  thinned-out  trachea  to  torsion.  Later  it  may  be  caused  by 
the  thinned-out  portion  being  sucked  down  into  the  trachea  at 
inspiration,  acting  as  a  valve,  or  by  edema  or  hemorrhage 
around  it  causing  it  to  collaiDse. 

The  symptoms  are  increasing  dyspnea  and  cyanosis,  the  ex- 
tent of  each  depending  on  the  degree  of  occlusion.  The  col- 
lapse is  apt  to  come  with  extreme  suddenness,  the  patient  dying 
with  scarceh^  a  struggle.  If  the  fact  that  the  trachea  is  com- 
pressed before  operation  is  determined,  measures  should  be 
taken  to  prevent  trouble  by  the  careful  manipulation  of  the 
gland.  A  tracheotomy  tube  should  be  at  hand.  If  there  is  a 
tendency  for  the  walls  of  the  trachea  to  fall  together,  this  may 
be  prevented  by  passing  a  suture  from  the  side  of  the  trachea  to 
the  edge  of  the  sternomastoid  muscle.  If  the  trachea  falls  to- 
gether despite  this  precaution,  tracheotomy  should  be  done  at 
once.  If  one  is  not  sure  as  to  the  permanence  of  the  patency,  it 
is  advisable  to  pack  the  wound  down  to  the  trachea  so  that 
tracheotomy  may  be  done  without  delay  should  disaster  impend. 

In  doing  a  tracheotomy  the  cut  edge  of  the  trachea  should 
be  sutured  into  the  overlying  muscles  or  skin  to  prevent  a 
second  collapse  should  it  be  necessary  to  remove  the  tube.  An 
experienced  nurse  should  be  in  constant  attendance.  In  a  few 
days  the  peritracheal  adhesions  fix  it  so  that  the  danger  of  re- 
newed collapse  is  past.  The  tube  should  be  removed  as  early  as 
possible  in  order  to  prevent  erosion  of  the  tracheal  mucosa 
which  is  more  liable  to  occur  in  these  cases  than  in  ordinary 
tracheotomies.  If  tracheotomy  does  not  relieve  the  symptoms 
at  once,  one  should  think  of  a  substernal  lobe  that  may  have 
been  partially  pulled  up  and  severed  from  the  rest  of  the  goiter 
during  the  operation. 

Hemorrhage 

Serious  hemorrhages  are  usually  due  to  the  slipping  of  a 
ligature  from  the  stump  of  a  large  vessel,  such  as  the  superior 


168  DISEASES    OF    THE    THYROID   GLAND 

thyroid  artery.  Cases  are  on  record  in  whicli  lieniorrhage  fol- 
lowed the  tearing  of  an  atheromatous  vessel  ruptured  after  liga- 
tion. When  such  a  large  vessel  becomes  patent,  there  is  a  rapid 
swelling  of  the  neck  with  a  rapidly  developing  dyspnea  and 
cyanosis,  but  without  the  sudden  appearance  of  symptoms  of 
tracheal  collapse.  The  symptoms  are  due  to  tracheal  pressure. 
Xot  sufficient  blood  can  escape  into  the  tissues  to  produce  any 
considerable  anemia.  The  wound  must  be  opened  and  the  bleed- 
ing vessel  caught  and  ligated. 

Hemorrhages  may  also  occur  from  small  vessels  being  over- 
looked during  the  operation,  from  their  ligatures  slipping,  by 
crushed  vessels  starting  to  bleed  again  after  the  forceps  have 
been  removed,  and  b}^  extensive  capillary  oozing.  Hemorrhages 
from  these  sources  may  or  may  not  cause  respiratory  difficulty. 
It  is  most  likely  to  happen  in  those  cases  where  the  tracheal  wall 
is  thinned  or  where  a  lobule  has  been  removed  from  behind  the 
trachea,  leaving  a  cavity  that  is  not  obliterated  by  Avound 
closure  but  which  subsequently  fills  with  a  clot.  If  the  wound 
has  been  drained,  these  slow  hemorrhages  seldom  give  trouble, 
if  it  has  not  been  drained  the  neck  may  gradually  enlarge  and 
the  dyspnea,  cyanosis  and  restlessness  appear.  Frequently  ooz- 
ing will  stop  spontaneously  and  treatment  is  not  needed.  If 
respiration  is  interfered  with,  the  wound  must  be  opened  at 
some  point  and  allowed  to  drain.  It  may  be  even  necessary  to 
insert  the  finger  to  remove  a  clot  which  may  be  exerting  pres- 
sure on  the  trachea. 

Hoarseness,  Loss  of  Voice,  Paralysis  of  Vocal  Cords 

Hoarseness  or  loss  of  voice  coming  on  gradually  in  from  a 
few  hours  to  a  few  days  after  operation  need  cause  no  alarm. 
When  coming  on  secondarily,  it  is  due  to  pressure  on  the  recur- 
rent laryngeal  nerve  caused  by  edema  and  infiltration  of  the  tis- 
sue, a  slow  capillary  oozing,  or  combinations  of  these.  Nothing 
need  be  done  as  the  condition  usually  clears  up  by  the  time  the 
patient  is  ready  to  leave  the  hospital.  In  some  instances  three, 
six  or  even  nine  months  may  be  required  before  the  difficulty 
disappears. 

If  vocal  cord  irritation  is  observed  during  the  course  of  the 
operation,  as  is  possible  when  using  a  local  anesthetic,  the  ma- 


HOSPITAL    MAXAGEMEXT    OF   GOITER   PATIEXTS  169 

iiipnlations  wliicli  cause  it  must  be  avoided.  If  the  irritation 
first  becomes  noticeable  immediately  after  operation  under 
general  anestliesia,  there  is  a  likelihood  that  actual  injury  of  the 
recurrent  laryngeal  nerve  has  occurred.  The  nerve  may  be 
crushed,  stretched,  torn,  cut  or  tightly  ligated.  If  crushed, 
ligated  or  stretched  there  is  a  possibility  of  spontaneous  restora- 
tion of  function  after  some  months,  depending  on  the  degree  of 
injury.  If  cut  or  torn  the  corresponding  vocal  cord  is  paralyzed 
and  the  damage  beyond  repair.  The  only  consolation  in  this 
case  is  the  fact  that  the  uninjured  vocal  cord  has  a  tendency  to 
compensate  for  the  loss  of  its  fellow,  and  after  some  time  and  in 
some  cases  the  voice  is  practically  restored  to  normal.  If  the 
paralysis  of  the  cord  was  known  to  have  existed  before  the  op- 
eration it  will  be  a  source  of  comfort  to  the  surgeon  though  this 
evidence  may  fail  to  convince  the  jury. 

Shock 

The  earlier  papers  on  after-course  gave  much  space  to  the 
discussion  of  shock.  Marked  shock  following  thyroidectomy  is 
now,  however,  an  unusual  occurrence.  Inhalation  anestliesia  is 
being  rapidly  replaced  by  local  anesthesia  for  goiter  surgery, 
as  the  excessive  loss  of  blood  incident  to  it  was  probably  respon- 
sible for  much  of  the  shock  then  seen.  In  addition  to  the  use  of 
local  anesthesia,  better  judgment  as  to  the  time  to  operate,  more 
thorough  preparation  of  the  patient  for  operation,  and  the  in- 
crease in  technical  skill,  all  tend  to  minimize  the  cases  of  shock. 

Real  shock  has  not  been  observed  following  goiter  opera- 
tions. I  have  frequently  noticed  toward  the  close  of  a  goiter 
operation  the  patient's  face  becomes  pale  and  covered  with 
beads  of  perspiration.  When  they  reach  their  room  the  pulse  is 
somewhat  rapid  and  weak.  These  are  cases  of  mild  degree  of 
shock.  On  being  placed  in  a  warm  bed,  surrounded  with  hot- 
w^ater  bottles  and  quieted  with  a  little  codeine  or  morphine  these 
symptoms  soon  passed  away  without  further  treatment. 

Acidosis 

In  the  extremely  toxic  cases  of  degenerative  goiter,  acido- 
sis is  sometimes  observed.  The  s>miptoms  appear  in  from  one  to 
six  days  after  operation.    The  patient  complains  of  being  des- 


170  DISEASES    OF    THE    THYROID   GLAND 

perately  sick  without  making  any  definite  complaint.  He  looks 
desperately  ill,  restless  and  irritable;  the  face  and  lips  are  pale, 
the  skin  cold  and  moist,  but  the  face  may  be  flushed,  with  a  hot 
dry  skin.  The  eyes  are  sunken,  pulse  rapid  and  weak,  tempera- 
ture elevated.  Vomiting  is  usually  present  at  some  time  and 
there  are  often  intervals  of  apathy  alternating  with  restless, 
or  even  active  delirium.  The  breath  has  a  distinct  acetone  odor. 
Finally  the  patient  passes  into  coma  with  Cheyne-Stokes  respira- 
tion and  dies. 

The  prophylactic  treatment  consists  of  avoiding  the  use 
of  drastic  hydragogue  cathartics  before  operation,  and  con- 
tinuing the  feeding  and  fluid  intake  of  the  patient  up  to  the  time 
of  operation.  AVhen  an  acidosis  is  imminent  6  to  12  gm.  of  soda 
bicarbonate  should  be  given  daily  for  two  to  three  days  preced- 
ing the  operation  and  carbohydrates  may  be  pushed  by  giving 
150  to  200  gm.  daily  of  lactose  in  lemonade  or  peppermint  water 
for  several  days  preceding  operation. 

A  minimum  amount  of  anesthetic  should  be  used  and  as 
little  trauma  as  possible  inflicted  at  operation.  Carbohydrate 
food  and  fluids  should  be  started  immediately  after  operation 
even  if  there  is  some  vomiting.  The  patient  should  be  given  a 
5  per  cent  sodium  bicarbonate  and  10  per  cent  glucose  solution 
in  normal  saline  by  proctoclysis. 

When  the  symptoms  are  well  developed,  a  2  per  cent  soda 
bicarbonate  solution  and  2  per  cent  glucose  in  normal  saline 
solution  should  be  given  subcutaneously,  and  where  the  case  is 
urgent,  1  gm.  each  of  soda  bicarbonate  and  glucose  and  .3  gm. 
of  noncrystalline  calcium  chloride  in  1000  c.  c.  of  normal  saline 
solution  may  be  given  intravenously  and  repeated  as  needed. 
Morphine  should  be  given  hypodermically  partly  to  conserve 
the  patient's  strength  and  also  because  it  seems  to  have  some 
specific  action.  Sodium  bicarbonate  should  be  constantly  pushed 
by  mouth,  12  to  20  gm.  daily  until  the  condition  improves. 

Infection 

AVith  the  present  day  operating  room  conditions  and  tech- 
nic,  infection  is  not  common.  When  it  does  occur  it  is  slight 
and  merely  delays  healing  and  results  in  more  disfiguring  scars. 

Infection  may  be  simulated  by  blebs  which  appear  a  day  or 


HOSPITAL   MAXAGEMEXT   OF   GOITER  PATIEXTS  171 

two  after  oi^eration  in  the  line  of  incision.  These  are  due  to 
tlie  irritation  of  the  iodine  on  the  delicate  skin  of  the  neck. 
These  blebs  may  be  opened  and  drained. 

If  drainage  was  instituted  at  the  time  of  operation,  this 
may  prove  sufficient  if  the  wound  has  not  closed  after  removal 
of  the  drainage  material.  If  no  drainage  was  placed  after  oper- 
ation, the  wound  edges  should  be  gently  separated  with  forceps. 
The  infection  is  nearly  always  confined  to  the  subcutaneous  fat. 

Deep  infection  may  not  show  up  early,  in  fact  areas  of 
fluctuation  may  not  appear  for  a  week  or  more.  It  should  be 
susjDected  whenever  a  part  of  the  incision  remains  swollen,  in- 
durated and  tender  and  the  temperature  remains  elevated.  I 
have  seen  low  grade  infections  overlooked  and  open  spontane- 
ously on  the  day  set  for  the  patient  to  leave  the  hospital.  This 
is  embarrassing,  and  when  the  above  conditions  are  present,  the 
prognosis  as  to  the  date  of  discharge  from  the  hospital  should  be 
guarded.  Whenever  the  drainage  of  deep  infection  is  made  the 
incision  should  be  spread  at  the  point  nearest  the  infection  and 
drainage  provided.  Hot  moist  dressings  applied  to  the  wound 
after  drainage  has  been  established,  hasten  the  evacuation  of 
the  pus  and  speed  healing. 

Sometimes  there  is  a  thickening  of  the  skin  and  subcu- 
taneous tissue  due  to  irritation  of  the  anesthetic.  This  is  most 
likely  to  appear  when  the  adrenalin  used  has  become  decom- 
posed as  may  be  noted  by  the  pink  color  of  the  solution.  This 
thickening  should  not  be  confused  with  an  infection.  It  disap- 
pears after  a  number  of  weeks  without  treatment.  The  disap- 
pearance may  be  expedited  by  the  application  of  hot  compresses. 

Disfiguring  Scars 

Scars  may  be  unsightly  because  of  their  breadth  or  because 
of  their  attachment  to  underlying  structures,  causing  annoyance 
to  the  patient. 

Bad  scars  may  be  caused  by  poor  approximation  of  the 
skin  at  operation,  but  more  frequently  result  from  w^ound  infec- 
tion and  subsequent  drainage  of  abscesses  or  because  of  the 
necessity  for  draining  the  wound  at  time  of  operation.  There 
are  a  certain  number  of  cases  which  develop  thick  red  keloid- 


172  DISEASES    OF    THE    THYROID   GLAND 

like  scars  when  approximation  has  been  perfect  and  healing  by 
primary  union. 

Scars  attached  to  the  trachea  or  larynx  often  cause  a  sense 
of  pulling  whenever  the  patient  swallows,  w^hich  is  in  some  cases 
extremely  annoying  to  the  patient.  It  also  produces  a  dimpling 
in  the  skin  or  a  pulling  upward  of  the  scar  which  a  sensitive 
patient  dislikes. 

The  preventive  measures  are  accurate  approximation  of 
the  skin  edges,  careful  asepsis,  removal  of  the  drainage  in 
twenty-four  to  forty-eight  hours  and  accurate  hempstasis  to 
avoid  the  necessity  for  drainage. 

The  use  of  fine  suture  material  and  its  removal  by  the 
fourth  day  after  operation  prevents  scarring  from  the  cutting 
in  of  sutures. 

Bronchitis  and  Pneumonia 

Pulmonary  complications  have  in  our  experience  proved 
one  of  the  rarest  complications,  even  bronchitis  being  seldom 
encountered. 

Tetany 

Tetany  is  a  definite  clinical  syndrome  resulting  from  a  sus- 
pension or  disturbance  of  parathyroid  function.  No  case  has 
been  observed  in  this  hospital.  It  was  much  more  common  as 
a  complication  in  those  days  of  complete  lobectomy.  As  it  is 
now  most  commonly  seen,  it  is  due  to  a  disturbance  of  the  nerve 
or  vascular  supply  of  the  parathyroids,  the  symptom  lasting 
from  a  few  hours  to  a  few  days.  As  there  is  some  variation  in 
the  size,  number  and  location  of  these  glands,  there  is  still  always 
a  possibility  of  tetany  even  when  the  posterior  capsule  and  some 
thyroid  tissue  is  left  at  operation.  Anything  interfering  with 
the  inferior  thyroid  arteries  might  affect  the  parathyroids  as 
this  is  the  source  of  their  blood  supply. 

The  symptoms  usually  appear  from  1  to  3  days  after  opera- 
tion. Stiffness  of  the  fingers  is  the  first  thing  noticed,  and  later, 
tonic  and  intermittent  contractions  of  the  flexor  muscles  of  the 
upper  extremities,  and  later  still  in  a  lesser  degree  of  the  lower 
extremities.  In  the  more  severe  cases  contraction  becomes  gen- 
eral, involving  the  muscles  of  the  esophagus,  masseter  muscles, 


HOSPITAL   MANAGEMENT   OF  GOITER   PATIENTS  173 

tongue,  larjmx,  and  diaphragm.  Death  is  caused  by  spasm  of 
the  diaphragm  or  glottis.  Heart  and  respiratory  rate  are  in- 
creased before  and  during  the  convulsion,  and  the  patient  is 
pale  due  to  vasoconstriction  until  the  cyanosis  of  diminished 
respiratory  function  appears. 

On  the  other  hand,  the  symptoms  may  disappear  spontane- 
ously in  a  few  hours,  or  in  a  few  days,  if  the  fmiction  of  the 
parathyroids  is  restored  by  compensatory  blood  supply,  or  other 
conditions  affecting  them  are  removed.  In  rare  instances  the 
condition  becomes  chronic. 

Calcium  lactate  given  orally,  rectally,  subcutaneously,  or 
intravenously  is  a  specific;  0.6  gm.  in  100  c.c.  of .  normal  saline 
gives  rapid  results,  and  it  should  be  given  so  in  severe  cases. 
In  others  the  slower  method  of  administration  suffices.  The 
treatment  should  be  repeated  if  the  symptoms  return.  This 
treatment  only  tides  the  patient  over  until  parathyroid  function 
is  restored. 

Myxedema 

Myxedema  is  a  rare  complication  after  thyroid ectomj^  It 
is  caused  by  too  much  of  the  thj^roid  tissue  being  removed 
or  by  a  later  disappearance  of  what  at  the  time  of  operation 
was  entirely  sufficient  amount  of  normal  tissue.  It  has  been  re- 
peatedly proved  that  only  a  very  small  amount  of  normal  thy- 
roid tissue  with  sufficient  blood  and  nerve  supply  is  adequate 
to  carry  on  the  normal  function  of  the  gland. 

A  mild  myxedema  may  not  be  recognized,  in  fact  well-de- 
veloped cases  have  been  overlooked  for  a  long  time.  The 
subcutaneous  swelling  which  does  not  pit  on  pressure,  the  thick, 
dry,  rough,  pale  skin,  and  dull  listless  mental  state,  the  oblitera- 
tion of  the  facial  lines  of  expression  and  the  thick  lips  and 
nostrils,  are  symptoms.  There  is  a  progressive  gain  in  weight. 
The  temperature  is  usually  subnormal  and  the  pulse  slow.  The 
patient  complains  of  cold  when  others  are  comfortable. 

The  treatment  is  the  giving  of  thyroid  extract.  The  patient 
should  be  started  at  gr.  i  doses  three  times  daily  and  this  soon 
increased  to  gr.  ii.  It  may  have  to  be  still  further  increased. 
The  effect  is  seen  in  the  loss  of  weight,  the  increased  rate  of  the 
pulse,  increase  in  temperature  to  normal  and  the  different  facial 


174  DISEASES    OF    THE    THYROID   GLAND 

appearance.    Tlie  treatment  nsually  lias  to  be  carried  through- 
out life  with  intermissions. 

Boothby,  of  the  Mayo  Clinic,  says  that  1  mg.  of  thyroxin 
given  hypodermically  every  other  day  will  soon  bring  the  meta- 
bolic rate,  which  is  below  normal,  up  to  normal  and  that  after 
that  1.6  mg.  daily  by  mouth  will  keep  it  so. 

Instructions  at  Dismissal 

The  operation  of  thyroidectomy  in  toxic  goiter  but  removes 
a  part  of  the  tissue  that  is  producing  an  abnormal  secretion. 
The  removal  but  gives  nature  a  chance  to  repair  the  damage 
done,  thus  the  cure  is  only  started  by  operation.  The  patient 
should  be  made  to  understand  that  she  should  not  expect  to  be 
well  in  a  few  weeks,  but  that  it  will  take  months  or  a  year  or 
more  and  that  the  rate  of  improvement  will  now  depend  almost 
entirely  on  her  own  conduct  in  the  future.  She  should  take 
regular  moderate  exercise,  preferably  in  the  open  air,  but  al- 
ways stop  short  of  fatigue.  She  must  avoid  the  excitement  of 
society  and  anything  else  that  produces  mental  excitement  or 
emotion.  Abundant  rest  is  necessary;  from  eight  to  ten  hours 
sleep  every  night  and  a  nap  during  the  day  is  desirable  for  the 
tirst  few  months.  A  plain  diet,  consisting  of  vegetables,  cereals, 
fruits,  milk  and  milk  products  is  best.  Meat  should  be  eaten 
very  sparingly ;  a  little  fish,  poultry  or  game  occasionally  is  most 
to  be  recommended.  Milk,  buttermilk,  abundance  of  water  is 
advised,  but  avoid  tea,  coffee,  and  alcohol. 


CHAPTER  VIII 

TREATMP]NT  OF  DISEASES  OF  THE  THYROID  GLAND 

Diseases  of  the  thyroid  gland  cover  such  a  wide  range  of 
possibilities  tJiat  in  determining  the  results  of  therapeutic  meas- 
ures it  is  necessary  to  proceed  with  the  most  rigid  self-criti- 
cism. The  fundamental  difference  between  recovery  and  cure 
is  nowhere  better  illustrated.  The  vast  number  of  measures  for 
its  ciiro  advanced  from  time  to  time,  and  tlie  results  alleged  to 
have  been  obtained,  are  proof  of  this  statement.  In  order  to 
judge  the  effect  of  a  therapeutic  measure  the  therapist  must 
have  a  thorough  knowledge  of  the  life  history  of  the  disease. 
The  disease  varies  so  much  that  it  is  exceedingly  difficult  to 
obtain  a  clear  notion  of  its  natural  course.  An  approximate 
picture  can  be  obtained  by  dividing  the  cases  in  their  several 
clinical  groups,  then  following  them  throughout  the  life  history 
of  the  individual,  a  requirement  obviously  difficult  to  fulfill. 

In  the  young  the  gland  is  often  enlarged,  and  often  disap- 
pears again  without  any  remedial  measures  having  been  ap- 
plied. In  many  of  these  the  enlargement  hardly  seems  beyond 
the  physiologic  and  tlie  cycle  might  l)e  regarded  as  a  normal 
one;  but  taken  as  a  group,  we  know  that  the  disappearance  is 
expedited  by  certain  measures.  Though  they  are  without  not- 
able symptoms,  their  disappearance  is  desired  lest  they  form  the 
basis  of  more  serious  disturbances  in  later  life.  Obviously  it  is 
of  importance  in  all  cases  in  the  adult  to  record  carefully  the 
various  changes  the  goiter  lias  undergone  up  to  the  time  of 
observation. 

Goiter  in  the  adult  is  a  dangerous  disease,  and  unless  cured 
tends  to  destroy  the  life  of  the  patient.  The  so-called  imiocent 
goiters,  which  frequentl}"  exist  for  ten  to  forty  years,  usually, 
sooner  or  later  kill  by  undergoing  toxic  or  malignant  degenera- 
tion. When  a  patient  is  first  observed  in  extremis  a  carefully 
worked  out  history  gives  the  observer  the  life  history  and  he  is 
then  enabled  to  determine  how  far  along  this  path  a  less  serious 
case  has  traveled. 

175 


176  DISEASES    OF    THE    THYROID   GLAXD 

The  cardiac  degenerations  associated  with  this  type  of 
goiter  are  generally  underestimated;  in  fact,  they  are  but  im- 
perfectly understood.  It  is  difficult  to  determine  whether  an 
existing  cardiac  condition  is  due  to  tlie  goiter  or  to  some  co- 
existent or  preexisting  cardiopathy.  Often  only  by  observing 
tiie  course  of  the  disease  under  treatment  can  this  point  be  deter- 
mined. 

There  is  no  other  disease  in  which  it  is  so  necessary  to  in- 
dividualize as  in  the  treatment  of  goiter.  A  close  and  usually  a 
protracted  study  is  necessary,  for  it  is  frequently  necessary  to 
shift  the  diagnosis  as  the  disease  progresses,  or  does  not  pro- 
gress, and  often  to  change  the  treatment  accordingly.  At  the 
first  meeting  the  plan  of  campaign  can  be  outlined  in  the  most 
general  terms  only.  Even  after  the  treatment  has  been  con- 
ducted to  an  apparently  successful  end,  observation  must  be 
continued.  The  need  for  this  is  obvious  when  we  remember  that 
at  most  we  modify  or  annihilate  but  a  part  of  the  disease.  It  is 
necessary,  therefore,  that  every  therapeutist  follow  his  cases 
and  construct  for  himself  a  series  of  experiences,  for  by  this 
means  alone  can  he  develop  the  niceties  of  judgment  so  neces- 
sary to  the  successful  treatment  of  goiter. 

After  operation  when  the  usual  improvement  follows,  the 
patient  is  apt  to  believe  that  she  is  cured  and  too  often  the  sur- 
geon shares  in  this  delusion.  It  should  be  remembered  that  the 
part  of  the  gland  the  surgeon  left  is  diseased  and  the  patient  is 
not  cured  until  this  has  been  restored  to  normal. 

In  the  following  account  only  the  broadest  outline  for  treat- 
ment can  be  constructed,  one  which  I  could  not  myself  follow 
^\dthout  the  aid  of  multitudinous  experiences  and  impressions 
impossible  to  commit  to  paper. 

Adolescent  Goiter 

In  this  type  there  is  but  a  mild  dysfunction,  characterized 
by  a  diffuse  enlargement,  usually  moderate  in  degree.  These 
nearly  always  respond  to  treatment  by  iodine.  Many  of  these 
disappear  spontaneously,  hence  one  must  regard  the  results  of 
this  therapeutic  measure  with  a  certain  degree  of  skepticism 
but  a  large  experience  by  countless  observers  has  established 
that  iodine  is  of  definite  value.    The  drug  may  be  given  in  the 


TREATMENT  177 

form  of  a  solution  of  iodine,  or  as  the  syrup  of  iodide  of  iron  or 
as  potassium  iodine.  The  form  selecteil  seems  to  be  of  no  moment. 
The  dose  required  is  small.  Because  of  the  more  pleasant  na- 
ture of  the  drug  my  preference  is  for  the  syrup  of  iodide  of  iron 
of  which  five  minims  may  be  giA^en  several  times  a  day. 

Iodine  nmst  be  given  over  long  periods  of  time  in  most  in- 
stances; months  or  even  a  year  or  more  are  often  required.  In 
young  children  the  result  is  usually  much  more  prompt. 

Iodine  externally  is  only  another  way  of  giving  the  drug 
and  is  an  unnecessary  though  harmless  adjunct.  If  the  patient 
or  her  mother  feels  that  it  is  necessary  to  do  penance  the  tincture 
of  iodine  may  be  smeared  on  externally. 

Thyroid  extract  works  more  promptly  than  iodine,  but  its 
action  must  be  more  carefully  control! etl  since  it  is  a  more 
powerful  agent.  The  dosage  must  be  small,  not  more  than  a 
grain  or  two  per  day  may  be  given. 

In  many  of  the  adolescent  goiters,  there  is  a  tendency  to 
hyperthyroidism,  hence  it  is  necessary  to  use  the  above  named 
agents  with  caution  so  that  if  toxic  symptoms  appear  the  drug 
can  be  promptly  discontinued.  They  may  be  given  iodine  until 
they  become  nervous  and  the  heart  rate  increases.  Then  the 
iodine  should  be  discontinued  and  sedatives  given  until  the 
nervousness  and  rapid  heart  subside.  Hyocine  and  bromides 
give  the  best  results.  From  4  to  6  minims  of  the  Fluid  Extract 
of  the  former  and  10  to  15  grains  of  the  latter  three  times  a  day 
usually  gives  good  results.  With  this  the  excitement  is  quieted 
and  the  iodine  may  be  resumed.  It  has  seemed  to  me  that  it  is 
possible  that  bromide  like  iodine  may  have  a  direct  specific  in- 
fluence on  the  gland  function.  By  following  this  plan  of  alter- 
nating iodine  and  sedatives,  many  may  be  conducted  to  recovery 
without  operation. 

These  youngsters  are  often  impatient  of  results  and 
clamor  for  operation  rather  than  undergo  the  prolonged  treat- 
ment necessarj^  for  a  medical  cure.  However,  one  should  not 
be  moved  by  these  pleadings,  for  if  a  cure  can  be  obtained  with- 
out operation  the  patient  likely  is  more  secure  from  future  diffi- 
culty than  if  a  part  of  the  gland  is  removed. 

In  some  of  the  adolescent  goiters  medical  treatment  does 
not  avail  and  operative  treatment  comes  into  question.    If  the 


178  DISEASES   OF   THE   THYROID   GLAND 

goiter  is  large  and  does  not  respond  to  treatment,  particularly 
if  the  family  is  predisposed  to  goiter,  operation  should  be  ad- 
vised. 

Those  which  tend  to  become  toxic  when  iodine  is  given 
even  though  a  prolonged  treatment  has  not  yet  been  tried  should 
be  considered  as  possibly  requiring  operation.  In  smaller 
goiters  which  are  very  sensitive  to  iodine,  early  operation  may 
be  required.  One  can  judge  only  by  noting  the  sensitiveness  to 
the  drug.  Some  complain  of  nervousness  and  congestion  in  the 
neck  with  the  very  first  dose  of  iodine.  Such  should  be  operated 
on  at  once. 

In  deciding  an  operation  for  adolescent  goiter  the  previous 
state  of  the  patient's  health  must  be  taken  into  account  as  well 
as  the  general  neuropathic  possibilities  in  the  family.  In  the 
neurotic  the  disturbance  from  the  exhibition  of  iodine  has  less 
significance  than  those  of  a  more  plethoric  heredity.  In  such 
cases  one  is  warranted  in  compromising  much  longer  than  in 
previously  robust  cases.  In  the  neurotic  the  result  of  operation 
is  not  satisfactory  for  even  if  they  are  cured  of  their  goiter  they 
will  be  neurotic  still.  If  there  is  a  neurotic  mother  the  unwar- 
ranted anticipation  of  a  regeneration  of  the  nervous  system  is 
apt  to  be  annoying  to  the  surgeon.  The  patient  after  operation 
will  be  no  better  than  she  was  before  the  advent  of  the  goiter. 
That  is  the  standard  upon  which  we  must  judge  our  therapeutics 
and  not  the  average  normal.  George  Ade  makes  the  wise  ob- 
servation that  if  the  young  swain  desires  to  know  what  shape 
the  daughter  will  have  at  fifty  to  study  the  profile  of  mother. 
Equally  so  if  one  desires  to  know  what  one  will  have  left  after 
curing  a  goiter  it  is  well  worth  while  to  study  the  mother.  Not 
only  heredity  but  environment  may  be  determined  from  such 
observation. 

Any  patient  who  is  taking  iodine  in  any  form,  or  the  thyroid 
extract,  must  be  carefully  vratched.  If  she  becomes  more  nerv- 
ous or  the  pulse  becomes  rapid,  this  line  of  medication  must  be 
stopped  and  a  sedative  substituted. 

It  is  not  advisable,  therefore,  to  give  the  patient  a  pre- 
scription and  allow  her  to  take  it  indefinitely  without  observing 
the  course. 

Often  these  patients  have  menstrual  disorders  which  ag- 


TREATMENT  179 

gravate  both  the  nervous  system  and  the  goiter  and  vitiate  the 
results  of  treatment.  Usually  these  individuals  are  substandard 
and  usually  slow  to  develop.  Something  may  be  done  by  general 
treatment,  hygienic  and  medicinal,  but  any  sort  of  operation 
on  the  pelvic  organs  but  makes  them  worse.  When  there  is 
marked  menstrual  disturbance  in  young  girls  who  have  goiters 
hydrastis  canadensis  with  iron  often  produces  excellent  results. 
Ten  minims  of  the  former  and  a  dram  of  the  elixir  iron,  quinine 
and  strychnine  is  a  convenient  form  of  giving  it.  Often  they 
marry,  and,  while  industriously  pushing  a  perambulator,  be- 
come forgetful  of  their  previous  complaints.  One  is  often  asked 
as  to  the  advisability  of  the  patient's  marrying  under  such  con- 
ditions. Advice  is  never  heeded,  of  course,  and  it  is  equally 
obvious  that  one  must  advise  against  marriage  in  substandard 
individuals,  but  it  is  a  comfort  to  know  that  since  the  advice  will 
be  ignored  the  patient  is  generally  improved  by  marriage. 
Hence  it  is  well  to  make  his  proscription  of  marriage  in  a  minor 
key. 

Colloid  Goiter  in  the  Adult 

It  is  the  exception  to  secure  any  noteworthy  results  by 
medication  in  the  colloid  goiter  of  the  adult.  It  happens  only 
in  the  transitional  type  between  the  adolescent  and  the  colloid. 
Occasionally  there  is  spontaneous  fluctuation  in  size,  particu- 
larly when  influenced  by  pregnancy,  and  in  rare  instances  some 
improvement  follows  iodine  medication.  On  the  other  hand, 
many  of  these  patients  are  made  markedly  worse  by  the  use  of 
iodine  or  thyroid  extract.  One  cannot  too  emphatically  warn 
against  the  use  of  agents  in  long  existent  stationary  goiter. 
Many  patients  are  started  on  their  downward  course  by  these 
agents  and  no  sedative,  operation  or  any  other  agent  can  rescue 
them  from  a  fatal  termination.  In  the  vast  majority  of  cases, 
operative  removal  is  the  only  measure  that  avails  anything. 
Personally,  I  categorically  refuse  to  treat  colloid  goiter,  even 
when  under  constant  observation,  other  than  by  operation.  To 
do  so  achieves  nothing,  and  it  but  encourages  those  patients  to 
regard  their  trouble  lightly. 

In  planning  an  operation  on  a  goiter  of  this  type,  usually 
there  is  a  mechanical  factor  to  be  considered.    Pressure  symp- 


180  DISEASES    OF    THE    THYROID   GLAND 

toms  must  be  relieved  as  a  first  consideration.  It  is  not  always 
easy  to  know  how  miieli  may  safely  be  removed.  A  considerable 
portion  of  each  lobe  should  be  removed.  The  operator  must 
judge  with  the  goiter  in  hand  how  much  it  is  safe  to  remove. 
Sometimes  relatively  normal  tissue  is  found  near  one  pole 
(usually  the  upper).  AVhen  this  is  the  case,  a  mass  the  size  of 
the  normal  lobe  is  all  that  is  required.  In  some  old  glands  there 
is  extensive  colloid  deposit  in  all  parts  of  the  gland.  In  such 
one  should  leave  a  larger  piece,  even  up  to  the  size  of  a  turkey 
egg,  preferably  at  tlie  left  upper  pole.  The  posterior  border  of 
each  lobe  should  be  left  whenever  possible,  because  this  usually 
represents  the  portion  of  the  gland  that  is  nearest  normal. 
Besides,  by  this  means  the  parathyroids  are  most  certainly  pro- 
tected. In  old,  very  much  calcified,  glands  it  sometimes  is  nec- 
essary to  do  a  complete  lobectomy  on  one  side  because  the  cal- 
careous infiltration  makes  a  resection  impossible.  The 
parathyroids  are  particularly  endangered  in  a  lobectomy  of  a 
calcareous  gland.  However,  if  the  parathyroids  are  certainly 
preserved  on  one  side,  the  patient  is  safeguarded. 

Early  operation  in  colloid  goiter  is  desirable  in  order  to 
avoid  the  consequences  of  degenerations  of  the  heart  and  ob- 
struction to  the  respiratory  passages.  The  chief  difficulty  we 
wish  to  avoid  is  the  subsequent  degeneration  into  a  secondary 
toxic  goiter.  If  we  remove  a  part,  is  the  remaining  portion  less 
likely  to  undergo  mischievous  change?  It  may  be  confidently 
said  that  it  is.  One  reason  for  this  is  that  the  most  pronoun- 
cedly degenerated  portion  is  removed.  Possibly  the  removal  of 
a  large  part  allows  that  remaining  to  become  restored  to  the 
normal  more  readily.  Medical  treatment  should  be  continued 
after  the  operation  with  the  idea  of  aiding  such  restoration. 
Our  knowledge  on  this  point  is  painfully  meager,  and  any  state- 
ment one  may  make  is  purely  hypothetical,  to  say  the  least. 

Unfortunately  on  this  fundamentally  important  problem  of 
subsequent  anatomic  change  we  are  without  trustworthy  in- 
formation. What  the  anatomic  state  of  the  remaining  part  may 
be  j^ears  after  an  operation  for  colloid  goiter  seems  not  to  have 
been  investigated.  Whether  malignancy  or  secondary  toxic 
goiter  develops  from  these  stumps  seems  not  to  have  been  deter- 
mined.   That  they  may  go  on  to  myxedema  is  well  known.  Per- 


TREATMEXT  181 

soiially  I  have  not  seen  nialig-nancy  or  secondary  toxic  goiter 
develoj)  after  resection  of  simple  colloid  goiter.  I  have  repeat- 
edly seen,  after  the  resection  of  one  lobe  for  a  mildly  toxic 
goiter,  the  other  lobe  develop  rapidly  and  produce  a  greater 
toxicity  than  the  one  previously  removed.  It  is  well  to  warn 
the  patient,  in  cases  where  there  is  one  large  lobe  that  is  toxic, 
that  after  the  removal  of  this  the  other  may  develop  and  pro- 
duce symptoms  and  that  this  in  turn  may  require  removal.  If 
one  does  not  thus  fortify  himself,  the  patient  is  very  apt  to  seek 
advice  elsewhere  when  the  relapse  comes. 

Primary  Toxic  Goiter 

In  considering  the  treatment  of  primary  toxic  goiter  it  is 
necessary  to  distinguish  between  the  various  types.  The  fetal 
adenomatous  toxic  goiter  is  always  a  surgical  disease  and  should 
be  attacked  as  soon  as  the  patient  is  in  a  proper  condition  for 
operation,  which  usually  is  as  soon  as  the  toxicity  is  recognized. 
Generally  speaking,  the  larger  the  goiter  the  better  the  results 
from  operation. 

In  the  frank  Basedow  with  goiters  of  considerable  size  the 
operation  is  necessary  and  satisfactory.  In  the  very  toxic  in 
Avhicli  the  goiter  is  A^ery  small  the  results  after  operation  are 
unsatisfactory.  If  the  patient  is  very  toxic,  preliminary  treat- 
ment is  necessary.  Rest  in  bed  and  bromides  constitute  the 
chief  treatment.  In  the  expansile  type,  pole  ligation  gives  good 
results. 

After  the  operation  the  patient  should  be  carefully  ob- 
served from  time  to  time.  Often  bromides  must  be  continued. 
If  other  portions  of  the  gland  enlarge  reoperation  may  be  nec- 
essar}^  A  toxic  goiter  history  is  complete  only  at  the  death  of 
the  patient.  In  the  intervening  period  symptoms  must  be  an- 
ticipated and  sought  for. 

Secondary  Toxic  Goiter 

It  has  already  been  stated  that  operation  should  be  advised 
in  all  colloid  goiters  in  adults.  When  these  show  evidence  of 
toxicity,  operation  should  be  urged.  Operation  is  indicated 
whenever  it  can  be  safely  employed.    If  there  has  been  marked 


182  DISEASES    OF    THE    THYROID   GLAND 

emaciation,  preliminary  treatment  must  be  instituted  until  the 
patient  begins  to  reg'ain  weight.  In  some  instances  there  may 
be  a  widely  dilated  heart,  requiring  rest  and  digitalis,  that  de- 
lays the  operation. 

If  there  is  not  a  gain  in  weight,  often  after  a  period  of 
stationary  weight,  operation  may  be  safe.  In  the  presence  of 
a  constantly  decreasing  weight,  operation  is  not  safe.  Such 
declines  cannot  be  halted  by  operation. 

In  general  the  preliminary  treatment  is  the  same  as  for 
the  primary  toxic  goiter,  but  usually  a  longer  period  of  treat- 
ment is  required. 

The  amount  of  gland  to  be  removed  depends  upon  the 
severity  of  conditions.  The  object  of  operative  treatment 
is  to  remove  as  much  as  possible  of  the  toxic  material.  The  re- 
moval of  one  lobe  was  formerly  generally  done,  later  the  re- 
moval of  a  part  of  both  lobes  was  advised.  The  objection  to 
the  complete  removal  of  one  lobe  is  that  the  recurrent  nerve  is 
more  frequently  injured.  The  removal  of  one  lobe  leaves  a  deep 
depression  over  the  site  of  the  removed  lobe  and  the  hump  of 
the  remaining  lobe  is  still  in  position.  The  removal  of  a  part 
of  both  lobes  preserves  the  posterior  part  of  each  which  protects 
the  nerve  and  parathyroid  glands  and  makes  the  removal  of  a 
larger  amount  of  gland  tissue  possible.  However,  I  believe  that 
in  very  toxic  goiters  where  the  preservation  of  life  is  the  one 
factor  in  mind,  one  had  best  do  a  lobectomy.  This  gets  rid  of 
a  maximum  amount  of  toxic  material  and  leaves  a  minimum  of 
oozing  tissue  and  inflicts  a  minimum  of  trauma  in  comparison 
to  the  amount  of  tissue  removed. 

The  amount  of  tissue  it  is  desirable  to  remove  in  this  type 
is  the  same  as  in  the  primary  toxic.  In  general  it  may  be  said 
that  a  piece  as  large  as  the  normal  lobe  should  be  left.  When 
too  much  is  removed,  deficiency  symptoms  may  result.  The 
deficiency  apparently  does  not  always  result  in  myxedema  but 
pronounced  general  disturbances  of  a  character  but  poorly  un- 
derstood are  not  infrequently  noticed. 

Generally  speaking  the  removal  of  a  part  of  the  gland  re- 
sults in  a  marked  improvement  of  the  s\Tuptoms.  The  improve- 
ment is  usually  more  marked  than  after  operations  for  primary 


TREATMENT  183 

toxic  goiters.  If  improvement  does  not  occur,  it  is  an  indication 
that  not  enough  of  the  gland  has  been  removed.  When  a  part 
of  the  ghmd  has  been  removed  and  the  improvement  is  but 
slight  and  transitory,  the  removal  of  an  additional  part  may 
produce  a  benefit  that  is  pronounced  and  permanent.  If  one 
lobe  only  apparently  is  enlarged  and  the  resection  of  this  does 
not  produce  satisfactory  results,  one  should  search  for  a  sub- 
sternal or  intrathoracic  lobe.  The  hidden  lobe  may  be  the  real 
offender.  An  aberrant  lobe  in  rare  cases  is  the  part  at  fault. 
When  patients  have  been  operated  on,  the  presence  of  enlarge- 
ment may  be  masked  by  the  scar  tissue.  This  is  particularly 
true  when  the  operation  has  been  badly  done  or  infection  has 
followed  operation.  In  these  cases  I  know  of  no  other  way  of 
finding  out  what  has  been  left  than  to  look  under  the  scar  and 
see.    Often  pressure  symptoms  maj  give  one  a  lead. 

In  the  very  toxic  patients  pole  ligation  may  be  done,  but 
it  is  less  likely  to  do  good  than  in  the  primary  toxic  goiter.  In 
fact  save  to  test  the  patient's  reaction  to  operative  procedures, 
I  believe  ligation  is  quite  useless. 

Interstitial  (Forme  Fniste) 

In  this  type  general  management  is  the  mainstay.  The 
avoidance  of  factors  which  tax  the  nervous  system  should  be 
advised.  General  hygienic  surroundings  are  desirable,  but  these 
patients  do  not  stand  physical  exercise  well.  They  tend  to  spon- 
taneous improvement  in  most  instances.  In  many  cases  they 
marry,  have  a  few  children,  then  lapse  into  semi-invalidism  even 
though  their  little  goiters  have  long  disappeared.  Usually  some 
form  of  a  sedative  is  desirable.  Small  doses  of  bromides  10  to 
15  grains  after  meals  with  or  without  hyoscyamus  (3  to  4 
minims  of  the  fluid  extract),  are  as  good  as  anything. 

Usually  there  is  disturbance  of  menstruation.  Measures 
which  improve  this  trouble  are  in  order.  Sometimes  there  is 
marked  retroflexion  of  the  uterus  the  definite  cure  of  which  by 
operation  is  advisable.  The  various  "local  treatments"  are  to 
be  condemned.  In  a  number  of  instances  I  have  noted  an  im- 
provement in  both  the  goiter  and  the  menstrual  disturbance  in 
patients  who  were  taking  pituitary  extract  (anterior  lobe)  in 
small  doses  (2  to  5  grains).    These  results  are  not  constant.    A 


184  DISEASES    OF    THE    THYROID   GLAND 

few  have  improved  with  corpus  luteuiii,  but  both  of  tliese  prepa- 
rations are  usually  disappointing. 

These  cases  are  combined  disturbances  most  likely,  the 
ovaries  and  possibly  other  organs  being  involved  as  well  as  the 
thyroid  gland.  Usually  the  one  is  as  incurable  as  the  other.  In 
my  early  experience  I  tried  to  remedy  the  condition  by  con- 
servative operations  on  the  ovaries.  The  results  were  not  re- 
assuring. Operation  on  the  goiter  I  have  found  disappointing. 
If  there  is  a  combination  with  adenomatous  goiter,  operation 
may  be  done  with  confidence  of  success.  If  the  goiter  becomes 
of  some  size  or  if  there  are  eye  signs  one  may  be  sure  that  the 
acini  have  multiplied  along  with  the  interstitial  cells  and  opera- 
tion is  indicated. 

With  the  various  nonoperative  procedures  for  the  destruc- 
tion of  gland  substance  I  have  had  no  experience.  Among  them 
may  be  mentioned  the  x-ray,  radium,  cauterization,  hot  water 
and  quinine  injections.  Each  of  these  has  had  its  warm  advo- 
cates. I  do  know  that  each  of  these  often  fail  and  that  they  ren- 
der operation  more  hazardous.  They  may  be  used  to  entertain 
the  patient  while  she  is  securing  the  necessary  rest.  In  order  to 
accomplish  this  purpose  it  is  not  necessary,  however,  to  employ 
them  vigorously  enough  to  increase  the  difficulties  of  operation. 


CHAPTER  IX 

TOPOGRAPHIC  ANATOMY  OF  THE  THYROID  GLAND 

The  region  of  interest  in  operations  on  the  thyroid  gland 
involves  the  most  complicated  region,  anatomically,  of  the  body. 
It  is  bounded  above  by  the  border  of  the  lower  jaw,  laterally 
by  the  sternomastoid  muscles  and  below  by  the  clavicles  and 
the  upper  border  of  the  sternum.  Adjacent  regions,  likewise, 
are  sometimes  invaded  by  the  gland,  and  the  surgeon's  interest 
and  activities  must  follow.  The  range  of  possibilities  is  so  great 
that  there  is  no  structure  in  the  neck  proper,  the  submaxillary 
and  substernal  regions,  but  that  may  at  some  time  become 
the  field  of  operation  for  goiter. 

Anatomical  points  will  be  considered  here  only  in  so  far 
as  it  is  necessary  to  the  presentation  of  the  typical  thyroidec- 
tomy as  performed  in  this  hospital. 

The  Overlying  Soft  Parts 

Before  the  gland  itself  can  be  discussed,  it  is  necessary  to 
consider  the  skin,  fascias  and  muscles  overlying  it. 

The  Skin  Covering 

The  skin  covering  the  neck  is  traversed  by  a  varying  num- 
ber of  folds  which  are  of  interest  to  the  operator  because  by 
following  them  with  his  incision  he  can  place  his  scar  so  that  the 
natural  folds  will  cover  it.  These  folds  consist  of  two  groups; 
an  upper  group,  varying  in  number  from  one  to  three,  which 
run  from  above,  medially  and  downward  about  the  level  of  the 
carotid  bifurcation,  following  in  a  general  way  the  direction  of 
the  lower  border  of  the  jaw.  These  lines  can  conveniently  be 
followed  in  the  incision  for  ligation  of  the  upper  poles.  When 
there  are  several  of  these  lines  the  one  most  completely  hidden 
may  be  selected.  The  second  group  of  folds  encircle  the  neck  at 
its  lower  part  just  above  the  sternum  and  clavicle.    The  lower 

185 


186  DISEASES    OF    THE    THYROID   GLAND 

lines,  if  several  exist,  can  be  used  for  the  collar  incision  which  is 
the  one  now  most  generally  made.  In  the  necks  of  old  women 
there  are  other  folds  higher  up  which  may  be  followed  con- 
veniently in  large  goiters.  If  these  folds  do  not  lie  just  at  the 
most  advantageous  point  for  the  incision  of  the  deeper  struc- 
tures, the  mobility  of  the  skin  is  such  that  it  may  be  easily  dis- 
placed to  make  the  deeper  field  easily  accessible. 

The  Platysma  Myoides 

The  platysma  myoides  covers,  in  a  radiating  manner  from 
above  downward  and  outward,  the  anterior  surface  of  the  neck 
(Fig.  70).  It  is  lost  above  over  the  border  of  the  jaw  in  the 
muscles  of  the  face  and  below  it  passes  out  of  the  field  of  inter- 
est by  losing  itself  in  the  pectoral  fascia  over  the  second  rib. 
It  lies  just  beneath  the  skin  and  is  rather  intimately  attached 
to  the  superficial  fascia.  The  chief  interest  of  the  platysma  to 
the  surgeon  is  that  it  serves  as  a  guide  to  important  veins.  In 
closing  the  wound  it  must  be  coapted  lest  its  traction  cause  an 
undesirable  widening  of  the  scar. 

The  Superficial  Veins 

Just  beneath  the  skin  and  in  front  of  the  superficial  fascia 
a  number  of  small  veins  are  found.  These  are  variable  in  num- 
ber and  each  subject  is  wholly  to  be  analyzed  for  itself.  They 
are  for  the  most  part  small  and  rarely  require  ligation  during 
operation.  The  platysma  often  contains  small  veins  that  require 
ligation. 

Just  beneath  the  cervical  fascia  the  jugular  veins  are  found. 
They  consist  of  the  external  jugular  veins,  which  do  not  usually 
fall  in  the  field  of  goiter  operations,  and  the  anterior  jugular 
veins  w^hicli  regularly  require  ligation  (Fig.  71).  These  chief 
veins  are  united  by  a  subsidiary  plexus  inconstant  in  arrange- 
ment. The  external  jugular  veins  extend  from  near  the  angle 
of  the  jaw  downward  and  lateralward  to  disappear  beneath  the 
clavicle  crossing  the  sternomastoid  muscle  near  its  middle.  In 
very  large  goiters  the  skin  incision  may  reach  these  vessels. 
The  anterior  jugular  veins  usually  lie  a  fingersbreadth  medial 
to  the  anterior  border  of  the  sternomastoid  muscle,  but  may  be 


TOPOGRAPHIC    AXATO-MY 


187 


0   '  ^    h      i  >ff  -  V-'^ 


Fig.  70. — The  fan-shaped  radiation  of  the  platysma  from  the  borders  of  the  jaws  to  the 
clavicles  is  shown.  IJetween  the  medial  borders  of  these  muscles  the  sternohyoid  muscles 
appear.  The  cervical  nerves,  lying  between  the  sternomastoid  and  platysma  muscles,  pass 
downward  and  medially.  The  relation  of  the  thyroid  gland  to  these  structures  is  shown  by 
the   dotted  figure. 


188  DISEASES    OF    THE    THYROID   GLAXD 

found  in  otlier  situations.  They  are  typically  two  in  number 
but  sometimes  six  or  more  may  require  ligation.  When  numer- 
ous they  are  found  at  irregular  points  between  the  borders  of 
the  two  muscles  above  mentioned.  They  are  readily  seen  shim- 
mering through  the  fascia  as  soon  as  the  skin,  subcutaneous  fat, 
and  platysma  have  been  severed.  There  is  usually  a  short 
branch  connecting  the  two  veins  just  above  the  clavicle.  When 
the  vessels  are  numerous,  connecting  branches  may  form  a  plexi- 
form  network.  If  care  is  exercised,  all  these  veins  can  be  recog- 
nized and  clamped  before  they  are  cut.  This  is  particularly 
easy  when  local  anesthesia  is  used. 

The  Muscles  of  the  Neck 

The  sternomastoid  muscles,  extending  from  the  inner  end 
of  the  clavicle  and  the  sternum  to  the  mastoid  process,  bound 
laterally  the  field  of  the  goiter  operations.  In  very  large  goiters, 
particularly  in  malignant  ones,  it  may  be  necessary  to  incise 
these  muscles,  but  ordinarily  they  can  be  retracted  out  of  reach 
of  the  knife.  Just  beneath  the  platysma  already  described  and 
between  the  two  sternomastoids,  the  sternohyoid  and  the  sterno- 
thyroid muscles  (Fig.  72)  lie.  Both  these  muscles  arise  from  the 
posterior  surface  of  the  upper  border  of  the  sternum.  The 
former  is  inserted  into  the  body  of  the  hyoid  bone  and  the  latter 
into  the  oblique  line  of  the  th^^roid,  cartilage.  This  arrangement 
brings  the  latter  to  lie  beneath  the  former.  When  the  thyroid 
gland  is  small,  these  muscles  are  unchanged,  but  when  the  gland 
is  large  they  are  flattened  into  ribbon-like  structures.  The  su- 
perficial ones,  the  sternohyoid,  have  intimate  fascial  attach- 
ments along  their  lateral  border  to  the  anterior  border  of  the 
sternomastoid  muscle.  It  is  the  severing  of  this  attachment 
that  does  much  to  give  free  access  to  the  gland  at  the  moment 
of  dislocation.  The  sternothyroid  muscle  lies  just  over  the 
gland,  being  separated  from  it  only  by  a  layer  of  connective  tis- 
sue, the  false  capsule  of  the  gland.  A  small  muscle  is  sometimes 
given  off  the  sternothyroid  which  extends  to  the  isthmus  of  the 
thyroid  gland  and  is  given  the  dignified  name  of  levator  gland- 
ulae  thyroideae.  It  assumes  importance  because  it  harbors  a 
small  artery  which  may  annoy  the  operator  if  it  is  severed. 


TOPOGRAPH IC    AXATOMY 


189 


These  muscles  obtain  tlieir  blood  supply  from  twigs  of  the 
cricothyroid  arteries.  These  vessels  are  small,  rarely  require- 
ing  ligation  in  operations  done  under  local  anesthesia.    There 


^  ^'^^ 


Hyold  bone  - 


Common  facial  vein 
..Thyroid  Cartilage 

Int.  jugular  vein 

I  )mohyoid  m. 


Ext.  jugular  vein 


Ant.  jugular  veins 


Ext.  jugular  vein 


Thyroid  gland  / 


Sternothyroid  m.  y 


Sternohyoid  m. 


Jugular  venous  arch 


Fig.  71. — The  relation  of  the  anterior  and  the  external  jugular  veins  is  shown.  The  ex- 
ternal He  over  the  sternomastoid  muscles  crossing  them  from  within  outward.  The  anterior 
veins  lie  medially  to  the  medial  border  of  the  muscles.  These  veins  lie  superficial  to  the 
short  muscles  of  the   neck.     The  position  of  the  thyroid  gland   is  shown  by   the   dotted   line. 

is  an  artery  which  courses  downward  at  the  median  edge  of  the 
sternomastoid  which  may  be  severed  when  the  sternohyoid  is 
separated  from  the  sternomastoid  muscles. 


190  DISEASES    OF    THE    THYROID   GLAND 

The  False  Capsule 

In  contradistinction  to  the  true  capsule,  mentioned  in  the 
section  on  histology,  the  false  capsule  must  be  distinguished. 
This  capsule  is  made  up  of  a  plane  of  fibrous  tissue  interposed 
between  tlie  true  capsule  of  tlie  gland  and  the  surrounding  struc- 
tures. In  front  it  is  a  more  or  less  definite  plane  lying  between 
the  true  capsule  and  the  posterior  surface  of  the  sternothyroid 
muscle.  Sometimes  it  is  so  intimately  blended  with  the  sheath  of 
these  muscles  that  it  cannot  be  separated  from  them.  Lateral 
to  the  gland  it  leaves  this  muscle  and  at  the  insertion  of  the 
middle  veins  divides  into  two  planes  (See  Fig.  94,  Chapter  X). 
The  one  follows  the  posterior  surface  of  the  gland  to  the  tra- 
cheal surface,  forming  attachments  for  the  gland  to  the  trachea, 
imbeds  the  parathyroid  bodies  and  the  recurrent  nerve  and  be- 
low is  continuous  with  the  prevertebral  fascia.  The  other  layer 
passes  outward  to  the  carotid  sheath  and  is  lost  in  the  fascia  of 
the  sternomastoid  muscle. 

The  Nerve  Supply  of  the  Skin  and  Muscles 

The  skin  in  the  anterior  surface  of  the  neck  is  supplied  by 
branches  of  the  superficial  cervical  nerves  (Fig.  73).  These 
nerves,  derived  from  the  second  and  third  cervical  roots,  curve 
first  backward  around  the  posterior  border  of  the  sternomastoid 
muscle  hence  forward  and  at  about  the  middle  of  this  muscle 
pass  between  it  and  the  external  jugular  veins,  perforate  the 
platysma  about  the  anterior  border  of  the  sternomastoid  and 
supply  the  skin  covering  the  anterior  surface  of  the  neck. 

The  skin  of  the  lower  portion  of  the  neck,  at  the  site  where 
the  usual  collar  incision  is  made,  is  supplied  in  part  by  the 
sternal  branches  of  the  supraclavicular  nerves.  These  nerves 
pass  behind  the  posterior  border  of  the  sternomastoid  muscle 
and  passing  under  the  jugular  vein  reach  the  supraclavicular 
region  over  the  clavicular  portion  of  the  sternomastoid  muscle. 

The  platysma  is  supplied  by  the  lower  branches  of  the  fa- 
cial nerve.  The  sternomastoid  muscles  are  supplied  by  branches 
from  the  spinal  accessory  nerve  while  the  sternohyoid  and 
sternothyroid  muscles  are  supplied  by  branches  from  the  de- 
scending branches  of  the  hypoglossal  nerves  and  from  deep 


TOPOGRAPHIC    AXATOMY 


191 


Mylohyoid  m 


Digastric  m. 


Submaxillary  gl 


Sup.  thyroid  art. 


Submaxillary  gl. 


Parotid  gl. 


Int.  jugular  v.  .,,- 


Common  carotid  art.- — """ 
Omohyoid  m 
Sternohyoid  m. 
Thyroid  gland 


it>  uid  bone 
Thyroid  cartilage 

Cricothyroid  m. 

Sternothyroid  m. 
Omohyoid  m. 


Sternocleidomastoid  m.*' 


Peetoraiis  maj.  m. 


Fig.  72. — The  sternomastoid  muscles  pass  obliquely  upward  and  outward  from  the  regrioa  of 
the  sternoclavicular  articulation  to  the  tip  of  the  mastoid  process.  Arising  from  the  posterior 
surface  of  the  upper  border  of  the  sternum  and  extending  to  the  hyoid  bone  are  the  sterno- 
hyoid muscles.  Beneath  the  lower  end  of  these  the  sternothyroid  muscles  are  seen.  The 
isthmus  of  the  thyroid  gland  appears  between  the  diverging  upper  extremities  of  these,  and 
the   cricothyroid    muscles   appear  just   above    the   isthmus. 


192 


DISEASES    OF    THE    THYROID   GLAND 


branches  of  the  first  tliree  cervical  nerves  forming  the  ansa  cer- 
vicalis. 

In  nerve-blocking  the  point  selected  is  wliere  the  nerves 


Descending  branch  of 
hypoglossal  n 


Sternooleidomastoid  m.- 

Omohyold  m 


Cutaneous  nerves  ol  neck 


Phrenic  n. 

Scalenus  ant.  m 


Sternothyroid  m. 


Sternohyoid  m. 


Fig.  73. — The  nerve  supply  of  the  neck.  The  anterior  cervical  nerves  are  seen  on  the 
right  looping  around  the  posterior  border  of  the  sternomastoid  muscle  and  radiate  medially 
and  downwards.  These  nerves  supply  the  skin.  On  the  left  of  the  figure  the  descending 
branches  of  the  hypoglossal  nerves  are  seen.  These  nerves  supply  the  deep  muscles  of  the 
neck. 

curve  around  the  posterior  border  of  the  sternomastoid  muscle. 
This  point  is  usually  about  on  the  plane  of  the  Adam's  apple. 


TOPOGRAPHIC   AN^ATOMY  193 

It  may  be  noted  that  blocking  these  nerves  does  not  affect  the 
nerve  supply  of  the  region  of  the  clavicles  nor  the  nerves  sup- 
plying the  dee  J)  muscles  of  the  neck. 

The  Nerve  Supply  of  the  Thyroid  Gland 

The  nerves  supplying  the  thyroid  gland  have  not  been  sat- 
isfactorily determined.  In  a  general  way  the  sympathetic,  the 
superior  lar\nigeal  and  the  recurrent  laryngeal  nerves  may  be 
said  to  be  distributed  to  the  gland. 

The  Sympathetic  Nerves 

Luschka  (Anatomic  des  menschlieben  Halses,  p.  306)  be- 
lieved those  nerves  reached  the  gland  only  by  following  the 
superior  thyroid  arterj^  Drobnik  (Arch.  f.  Anat.  u.  Entwick- 
lungsgesch.  Jahrg.,  1887,  S.  339)  believes  that  nerves  are  given 
off  from  the  second  cervical  ganglion  uniting  with  the  first  car- 
diac nerves  and  then  sending  branches  to  the  gland  along  the  in- 
ferior thyroid  arteries.  The  position  of  these  nerves  is  of  in- 
terest because  some  surgeons  think  the  destruction  of  this  nerve 
supply  is  the  factor  of  importance  in  pole  ligations. 

The  Superior  Larjmgeal  Nerves 

These  are  branches  of  the  lOtli  cervical  ganglia  of  the  sym- 
pathetic and  supply  the  mucous  membrane  of  the  larynx. 
Whether  the  thyroid  gland  receives  any  branches  from  them  has 
not  been  satisfactorily  demonstrated.  Lindeman  (Centralbl.  f. 
allg.  Path.  u.  path.  Anat.,  1891,  ii,  321)  believes  both  the  supe- 
rior and  recurrent  nerves  send  brandies  to  the  thyroid  gland. 

The  Recurrent  Lar3nigeal  Nerves 

These  nerves  ascend  from  the  thorax,  the  right  passing 
around  the  subclavian  artery,  the  left  around  the  aorta,  and  ap- 
proach the  cleft  betAveen  the  trachea,  esophagus  and  lower  pole 
of  the  thyroid  gland  (Fig.  76).  As  they  approach  this  region 
they  cross  the  inferior  thyroid  vessels,  sometimes  in  front,  some- 
times behind  and  sometimes  between  its  branches,  when  division 
takes  place  some  distance  before  the  gland  is  reached.  They  en- 
ter tlie  larynx  at  the  level  of  the  hyoid  bone  and  supply  all  the 


194  DISEASES    OF    THE    THYROID   GIxAND 

muscles  of  the  larynx  except  the  cricothyroid.  Drobnik  be- 
lieves the  recurrent  nerves  receive  branches  of  the  sympathetic 
nerves.  The  interest  in  this  nerve  lies  chiefly  in  the  fact  that 
it  is  liable  to  injury  in  lobectomy  or  in  careless  ligation  of 
stumps  in  lobe  resections. 

Topog^raphy  of  the  Gland 

The  thyroid  gland  is  a  bilobed  gland  joined  by  a  narrow 
isthmus.  Each  lobe  is  pear-shaped  and  lies  on  either  side  of  the 
trachea.  The  lobes  are  two  inches  long  and  extend  from  the 
lower  border  of  the  thyroid  cartilage  to  the  third  tracheal  ring 
(Fig.  74).  The  lateral  lobes  are  united  in  most  cases  by  an  isth- 
mus which  covers  the  second  and  third  tracheal  rings.  The  isth- 
mus is  said  to  be  absent  in  10  to  20  per  cent  of  the  cases.  I  have 
rarely  found  it  absent.  The  isthmus  is  united  to  the  trachea 
by  abundant  connective  tissue  bands,  the  ligaments  of  the  thy- 
roid gland.  Often  there  is  a  fascial  band  extending  from  the  thy- 
roid cartilage  to  the  isthmus.  This  is  the  suspensory  ligament. 
Sometimes  it  contains  a  few  muscular  fibers  as  already  noted. 
Often  an  elongated  mass  extends  upward  from  one  of  the  lobes, 
usually  the  left  and  may  reach  as  high  as  the  hyoid  bone.  This 
is  caJled  the  pyramidal  lobe  (Fig.  78).  The  median  borders  of 
the  lateral  lobes  are  united  to  the  trachea  by  fascial  bands. 
These  sometimes  contain  small  arteries.  At  the  posterior  inner 
border  of  the  gland  there  is  considerable  loose  areolar  tissue 
Avhicli  harbors  the  recurrent  laryngeal  nerve.  At  the  point 
where  the  thyroid  comes  in  close  contact  with  the  trachea  lime 
salts  may  become  deposited  uniting  the  goiter  firmly  to  the 
trachea  by  a  calcareous  bridge.  The  separation  of  such  bridges 
may  cause  some  difficulty  and  result  in  annoying  hemorrhage. 

The  Blood  Supply  of  the  Thyroid  Gland 

Descriptions  of  the  thyroid  gland  generally  begin  with  the 
statement  that  it  is  a  very  vascular  organ.  This  is  usually  the 
first  fact  the  young  surgeon  verifies  when  he  begins  .to  operate. 
A  thorough  knowledge  of  the  paths  through  which  this  gland 
receives  and  dispels  its  blood  does  much  to  lessen  the  pain  of 
tliis  first  lesson. 


TOPOGRAPHIC    ANATOMY 


195 


#  % 


/.■ 


Fig.  74. — The  general  topographic  relations  of  the  thyroid  gland.  It  straddles  the  upper 
portion  of  the  trachea  covering  the  upper  three  tracheal  rings.  The  upper  poles  overlie  the 
lower  edges  of  the  thyroid  cartilage.  The  carotid  vessels  lie  lateral  to  the  lateral  lobes.  The 
medial   borders   of   the   sternomastoid    muscles   cover   the   lateral    borders    of   the    lateral    lobes. 


196  DISEASES    OF    THE    THYROID   GLAND 

Generally  speaking,  the  thyroid  gland  is  supplied  by  two 
pairs  of  arteries  and  drained  by  corresponding  veins.  The 
number  of  veins,  however,  varies  considerably. 

The  Arteries  of  the  Thyroid  Gland 

The  principal  arteries  are  the  superior  and  inferior  thyroid 
arteries.  The  lesser  are  the  artery  to  the  suspensory  ligament 
and  the  thyroidea  ima  arteries. 

The  Superior  Thyroid  Arteries 

The  most  constant  vessels  are  the  superior  thyroid  arteries. 
They  arise  from  the  external  carotid  arteries  just  above  the 
bifurcation  of  the  common  carotid  arteries.  They  course  first 
upward  to  near  the  greater  cornu  of  the  hyoid  bone,  then  curve 
downward  and  medially  and  enter  the  upper  pole  of  the  gland 
just  anterior  to  the  summit  (Fig.  75).  Near  their  origin  they 
give  off  branches  which  course  along  the  medial  border  of  the 
sternomastoid  muscle,  and  more  medially  other  branches  which 
form  a  plexus  in  front  of  the  thyroid  cartilage  and  the  cricoid 
membrane.  The  superior  thyroid  artery  is  usually  about  the 
size  of  a  knitting  needle.  The  comparison  is  apt  because  the 
size  of  a  knitting  needle  varies.  When  there  is  a  large  goiter 
the  vessel  may  be  much  enlarged.  I  have  seen  it  larger  than  a 
normal  radial.  It  is  only  occasionally  that  it  is  small,  due  either 
to  a  maldevelopment  of  the  lobe  or  to  the  presence  of  a  large 
branch  of  the  superior  laryngeal  artery. 

The  Artery  to  the  Suspensory  Ligament 

The  superior  larjTigeal  artery,  itself  a  branch  from  the  su- 
perior thyroid,  sends  a  small  branch  to  the  suspensory  ligament 
or  the  pyramidal  lobe  as  the  case  may  be  (Fig.  75).  Sometimes 
it  extends  downward  as  a  considerable  branch  and  anastomoses 
with  the  posterior  branch  of  the  inferior  thyroid  artery.  The 
cricothyroid  arteries  are  branches  which  come  off  the  superior 
thyroid  arteries  at  the  level  of  the  cricothyroid  membrane  and 
by  uniting  form  an  arch.  Somewhere  from  this  arch  there  is 
usually  a  small  artery  which  descends  in  the  suspensory  lig- 
ament or  on  the  pja'amidal  lobe  if  one  exists.  This  is  the  artery 
to  the  suspensory  ligament. 


TOPOGRAPHIC    A^^ATOMY 


197 


Tills  small  vessel  deserves  the  attention  of  the  surgeon. 
Though  small,  when  the  tissue  in  which  it  lies  is  cut,  it  tends 
to  retract  and  may  be  the  source  of  considerable  hemorrhage, 
particularly  delayed  hemorrhage. 


Ext.  carotid 
art. 


Sup.  thyroid 
art. 


Thyroid 
cartilage 


Sup.  thyroid  vein__- 


Anterior  branch 


Cricothyroid  m. ,  _ 


Middle  thyroid 
vein 


Inf.  thyroid  vein 


Inf.  thyroid 
art.  ^ 


,  Sup.  thyroid  art. 


Sternomastold 
_  branch 


—  Sup.  thyroid  vein 


—  Com.  carotid  art. 


Int.  Jugular  vein 


'fl^if 


Subclavian  vein  / 

Subclavian  art.  / 

Thyroid  ima  art.  (var.i  y' 


~    Left  Innominate  vein 


_  Arch  of  aorta 


Fig.  75. — The  arterial  supply  of  tlie  thyroid  gland.  The  superior  thyroid  arteries  enter  the 
superior  poles  at  the  anterior  surface.  From  these  vessels  branches  extend  across  the  thyroid 
cartilage,  the  cricothyroid  arteries,  to  anastomose  with  their  fellows  of  the  opposite  side.  From 
these  a  branch  is  given  off  which  follows  the  pyramidal  lobe,  the  suspensory  ligament  or 
suspensory  muscle,  as  the  case  may  be,  to  the  isthmus  of  the  thyroid  gland.  The  inferior 
thyroid  arteries  are  derived  from  the  celiac  axis  and  passing  behind  the  carotid  vessels,  enter 
the  lower  pole   of   the   thyroid   gland.      (See   the   noxt   figure.) 


198  DISEASES    OF    THE    THYROID   GLAND 

The  Inferior  Thyroid  Arteries 

Tlie  lower  pole  is  supplied  by  the  inferior  thyroid  arteries. 
They  arise  from  the  thyroid  axis,  together  with  the  suprascap- 
ular and  the  transverse  cervical  and  ascend  upward  and  inward 
behind  the  sheath  of  the  common  carotid  artery  and  internal 
jugular  vein  and  approach  the  lower  poles  of  the  thyroid  gland 
at  the  point  of  maximum  convexity.  They  divide  before  they 
enter  the  gland;  the  one  following  the  lateral  border  plunges  at 
once  into  the  dejjtli  of  the  gland  (Fig.  76).  The  other,  the  in- 
ferior branch,  remains  more  superficial  and  continues  upward 
just  within  the  substance  of  the  gland  in  its  posteromedial  bor- 
der. From  this  branches  are  sent  forward  into  the  substance  of 
the  gland  and  anastomose  with  branches  of  the  arteries  of  the 
other  side  through  the  isthnnis  and  possibly  with  branches  from 
the  superior  laryngeal  arteries  (Fig.  76).  Some  anatomists  be- 
lieve there  is  a  direct  anastomosis  between  the  superior  and  in- 
ferior thyroid  arteries.  Ilyrtle  denies  such  anastomosis.  There 
is  reason  to  believe  that  this  is  correct,  for  when  the  superior 
thyroid  arteries  are  ligated,  the  upper  pole  can  be  cut  across 
without  causing  hemorrhage.  There  is  no  doubt  but  that  by 
far  the  larger  part  of  the  gland  is  supplied  by  the  inferior  thy- 
roid arteries.  The  vessel  sometimes  divides  some  distance  be- 
fore the  thyroid  gland  is  reached,  in  which  event  the  recurrent 
laryngeal  nerve  may  pass  between  the  two  branches.  The  in- 
ferior thyroid  arteries  vary  more  in  size  than  do  the  superior. 
The  artery  of  the  opposite  side  may  compensate  for  a  diminutive 
one.  The  site  of  division  and  the  number  of  branches  vary  con- 
siderably. It  is  even  more  prone  to  displacement  by  the  va- 
garies of  enlargement  of  the  gland  than  is  the  superior.  It  is  by 
the  posterior  branch  of  these  vessels  that  the  nutrition  to  the 
parathyroid  glands  is  conveyed.  These  vessels  likewise  give 
off  the  branches  to  the  trachea  which  sometimes  are  of  suffi- 
cient size  to  annoy  the  operator. 

The  Th3rroidea  Ima  Artery 

The  thyroidea  ima  artery  is  a  small  vessel  which,  accord- 
ing to  G  ruber,  occurs  in  one  case  in  ten,  springs  directly  from 
the  arch  of  the  aorta  between  the  anonymous  and  the  common 


TOPOGRAPHIC   ANATOMY 


199 


~t| —  Oesophagus 


Thyroid  gland 


Ext.  carotid 

art. 


Sup.  thyroid 
art.- 


Vagus  nerve 


Thyroid  gland 


Int.  jugular  v._ 


Inf.  thyroid      ,   ;  j' 
art. 


Sup.  thyroid 
--  art. 


Com.  carotid  art. 


Sup.  parathyroid 
gland 


Tracheal  and 
Oesophageal 
branches  ^^ 


Inf.  parathyroid 
gland 


_  Inf.  thyroid  art. 


Subclavian  art.^'' 


Trachea/ 


Recurrent  laryngeal 
nerves 


-  Sup.  vena  cava 


Fig.  76. — The  arteries  of  the  thyroid  gland  and  the  recurrent  laryngeal  nerve.  The 
sui)L'rior  thyroid  artery  is  seen  to  enter  the  superior  pole  anterior  to  its  apex.  The  inferior 
thyroid  arteries  arise  from  the  thyroid  axis,  ascend  first  upward  and  then  medially  behind 
the  common  carotid  arteries.  As  they  approach  the  gland,  they  divide  into  two  branches. 
The  one  enters  the  lower  lateral  border.  The  second  branch  passes  behind  the  lower  pole 
and  enters  the  gland  near  the  medial  border.  It  ascends  to  the  midpoint  of  the  gland  and 
then  enters  deeply  into  it.  The  recurrent  laryngeal  nerves  ascend  along  the  lateral  surlacc 
of  the  trachea  to  the  cricothyroid   membrane. 


200  DISEASES    OF    THE    THYROID   GLAND 

carotid  artery.  It  reaches  the  isthmus  of  the  thyroid  gland  by 
traveling  in  front  of  the  trachea  verging  slightly  from  left  to 
right. 

Disturbance  of  the  Site  of  the  Vessels  by  Thyroid  Hypertrophy 

As  the  lobes  enlarge,  the  gland  is  subject  to  a  great  variety 
of  disturbances  in  position,  particularly  when  the  enlargement 
of  the  gland  is  irregular  and  bosselated.  Because  of  this  the 
relation  to  the  various  adjacent  structures  may  be  very  mate- 
rially altered.  Enlargement  toward  the  medial  line  may  com- 
press the  trachea,  producing  a  flattening,  the  so-called  "saber 
sheath"  trachea,  or  if  there  is  irregular  enlargement  of  the  ad- 
jacent lobe,  the  trachea  may  be  curved  to  accommodate  itself  to 
such  enlargement.  Because  of  such  deformities  the  lumen  of 
the  trachea  may  be  very  much  lessened. 

The  growth  of  the  lobulations  in  directions  other  than  to- 
ward the  trachea  leads  to  displacement  of  vessels.  When  this 
occurs  at  the  upper  pole  the  superior  thyroid  vessels  are  dis- 
placed. When  a  lobulation  occurs  lateral  to  the  vessels  they 
are  displaced  toward  the  median  line  (1,  Fig.  77).  This  displace- 
ment may  be  so  great  as  to  push  the  vessels  beyond  the  median 
line.  If  a  lobe  develops  medial  to  the  vessels  they  may  be 
pushed  far  laterally  {2,  Fig.  77)  and  sometimes  carried  high 
upon  the  neck.  Such  wide  deviations  may  cause  the  surgeon  to 
miss  the  main  vessel  in  the  ligation  and  tie  a  minor  one. 

Lateral  lobulations  may  extend  beyond  the  site  of  entrance 
to  the  median  vein  leaving  a  constriction  of  fibrous  tissue  at  the 
site  of  the  vein,  which  partly  subdivides  the  lobes  into  lobuli  (4, 
Fig.  77).  The  failure  to  recognize  the  importance  of  these  sep- 
tae  Avill  cause  the  surgeon  to  lose  the  line  of  cleavage.  The  sep- 
tae  often  carry  vessels  of  importance  and  if  severed  and  allowed 
to  contract  may  give  rise  to  troublesome  hemorrhages. 

The  lower  pole  more  than  the  upper  is  liable  to  marked  dis- 
placement. The  vessels  are  often  displaced,  the  veins  medially 
and  the  artery  downward  {8,  Fig.  77).  The  displacement  down- 
ward behind  the  clavicle  constitutes  the  most  common  displace- 
ment and  produces  the  common  substernal  goiter.  Because  of 
tlie  close  relation  of  this  to  the  intrathoracic  and  other  aberrant 
lobes,  these  are  discussed  in  a  separate  chapter. 


TOPOGRAPHIC    AXATOAEY 


201 


Fig.  n, — Aberrant  locations  of  the  thyroid  arteries.  (1)  The  superior  thyroid  artery  is 
displaced  medially  by  an  unusual  development  of  the  superior  pole.  (2)  The  superior  thyroid 
artery  is  displaced  laterally  by  the  medial  development  of  the  superior  lobe.  (3)  The  inferior 
thyroid  artery  is  displaced  medially  by  a  massive  development  of  the  lower  pole.  (4)  The 
inferior   thyroid   artery   is  displaced   upward  by  a  marked   hypertrophy  of  the   lower  pole. 


202  DISEASES    OF    THE    THYROID   GLAND 

The  Thyroid  Veins. — Tlie  efferent  cliannels  of  the  thyroid 
gland  are  numerous  and  tliin  walled.  They  leave  the  gland  at 
three  chief  points,  the  upper  pole,  the  middle  of  the  lateral  sur- 
face, and  the  lower  pole. 

Superior  Thyroid  Vein  is  usually  single  and  leaves  the 
gland  usually  at  the  level  of  the  upper  pole  along  with  the  ar- 
tery (Fig.  78). 

The  Middle  Thyroid  Veins  arise  from  the  lateral  border  of 
the  lobes  and  pass  directly  lateralward  and  empty  into  the  in- 
ternal jugular  veins  (Fig.  78).  Often  there  are  two  or  more. 
If  there  are  several  the  supernumerary  ones  usually  come  off 
nearer  the  upper  pole.  These  middle  thyroid  veins  are  often 
torn  by  the  surgeon  in  enucleating  the  gland.  This  is  the  most 
common  source  of  troublesome  hemorrhage. 

The  Inferior  Thyroid  Veins  come  off  from  the  lower  pole 
near  the  median  border.  In  the  beginning  they  are  three  or 
four  or  more  in  number  but  usually  collect  into  two  main  trunks, 
the  inferior  thyroid  and  the  thyroidea  ima  veins  (Fig.  78).  The 
first  passes  downward  and  lateralward  and  empties  into  the  in- 
ternal jugular,  the  other  into  the  innominate  vein  just  in  front 
of  the  origin  of  the  common  carotid  artery.  On  the  left  side 
both  veins  pass  downward  and  to  the  left  and  empty  into  the 
left  innominate  vein.  If  there  is  a  pronounced  enlargement 
of  one  lower  lobe  only,  these  veins  may  be  carried  in  front  of 
the  trachea  or  even  to  the  opposite  side.  The  veins  arising  from 
the  lower  pole  often  form  a  considerable  plexus.  Because  of  this 
the  size  and  situation  of  the  veins  is  very  variable.  These  ves- 
sels are  often  closely  attached  to  the  false  capsule  of  the  gland, 
making  careful  dissection  at  this  point  very  important. 

The  Thyroidea  Ima  Vein,  when  present,  arises  in  the  venous 
plexus  over  the  isthmus  and  passes  dow^nw^ard  in  front  of  the 
trachea  and  empties  in  the  left  innominate  vein. 

Typical  Sites  of  the  Ligation  of  Vessels. — There  are  several 
points  of  election  in  the  ligation  of  the  veins  (Fig.  79).  The 
first  point  is  at  the  superior  pole.  By  ligating  the  vessels  just 
above  the  superior  pole,  or  by  ligating  the  point  of  the  gland 
itself,  the  upper  pole  is  made  bloodless.  The  lateral  veins  if 
double-clamped  permit  the  rotation  medially  of  the  lobe  without 
the  loss  of  blood.     The  inferior  thyroid  artery  can  usually  be 


TOPOGRAPHIC    AXATOMY 


203 


Digastric  m.\ 
\ 
\ 

Hyoid  bone  ,,  \ 


Masseter  m. 


Mylohyoid  m. 

parotid  gland 

Ant.  facial  vein 


Sup.  thyroid 
art.  and  vein 


Thyroid  cartilage 


Sternocleidomastoid  m 


Middle  thyroid  vein 
Inf.  thyroid  vein_^ 


Common 
carotid  art 


Inf.  thyroid  vein 


Vagus  nerve  . 


\  Vagus  nerve 

Inn'<minate  vein 


roid  ima  veins 


Sup.  veua  cava 

Fig."  78. — The  veins  of  the  thyroid  gland.  The  veins  of  the  upper  part  of  the  gland 
collect  at  the  upper  pole  and  leave  as  a  single  trunk.  At  the  lateral  border  the  median  veins 
empty  into  the  internal  jugular  veins.  At  the  lower  pole  the  inferior  jugular  veins  empty 
into    the   internal   jugular  and   the   thyroidea    ima   veins   empty   into    the    innominate  vein. 


204  DISEASES    OF    THE    THYROID    GT.AXD 

seen  at  the  lateral  border  of  tlie  lower  pole.  By  passing  a  suture 
through  the  gland  this  vessel  can  be  occluded.  The  veins  aris- 
ing in  the  lower  ])ole  can  })e  contiollod  ))y  a  single  ligature.  The 
medial  branch  of  the  inferior  thyroid  artery  can  be  clamped  at 
the  moment  it  is  cut  within  the  substance  of  the  gland.     This 


Fig.  79. — Typical  sites  for  ligation  of  the  thyroid  vessels.  The  superior  thyroid  vessels 
are  ligated  en  masse  with  the  tip  of  the  upper  pole.  The  lateral  veins  are  ligated  between 
the  gland  and  the  internal  jugular  veins.  The  inferior  thyroid  arteries  are  ligated,  when 
they  divide  before  entering  the  gland,  the  upper  as  it  enters  the  gland,  and  the  lower  in  the 
middle  of  the  gland  after  being  cut  in  the  resection  of  the  gland.  The  inferior  veins  may 
be   ligated   separately  or   en   masse   depending  on    their   relation   to   each   other. 

preserves  that  portion  of  the  artery  which  supplies  the  para- 
thyroid glands.  By  following  this  scheme  the  greater  part  of 
the  blood  supply  can  be  excluded  before  the  substance  of  the 
gland  is  cut  into.  This  simplifies  the  technic  and  lessens  the 
hemorrhage  materially. 


CHAPTER  X 

TECHXIC  OF  OPERATIONS  ON  THE  THYROID  GLAND 

Operations  on  tlie  thyroid  gland  involve  many  of  the  finer 
points  in  surgical  technie.  The  thinness  and  abundance  of  the 
vessels  and  the  proximity  of  important  nerves  are  the  chief  fac- 
tors which  demand  accuracy  and  delicate  technie.  The  gland  is 
separated  by  delicate  layers  of  connective  tissue  from  the  sur- 
rounding structures,  therefore  an  accurate  determination  of  the 
line  of  cleavage  makes  for  a  good  operation.  Patency  of  the 
tracheal  lumen  nuist  be  maintained  and  when  this  structure  is 
compressed  and  displaced,  by  tlie  irregular  growth  of  the  gland, 
careful  manipulation  and  constant  observation  of  the  patient's 
respiratory  function  are  demanded.  Accurate  approximation  is 
required  to  retain  the  synnnetry  of  the  neck  and  to  avoid  an  un- 
sightly scar. 

Like  all  major  operations  on  the  neck,  a  constant  atten- 
tion to  hemostasis  is  demanded.  A  vessel  that  will  eventually 
require  ligation  should  be  tied  at  once.  It  requires  no  more  time 
to  do  it  at  once  than  to  do  it  later  and  the  possibility  of  tearing 
off  a  vessel  by  an  unintentional  pull  on  a  clamp  is  removed  and 
the  field  of  operation  is  not  obstructed  by  a  lot  of  artery  clamps; 
besides  the  forceps  are  released  for  use  again.  A  dozen  forceps 
are  enough  for  any  operation.  The  safest  cutting  instrument 
to  use  in  dangerous  areas  is  a  sharp  knife.  The  scissors  have  no 
place  in  goiter  operations  except  for  the  cutting  of  ligatures. 

Many  complicating  factors  may  appear  in  goiter  surgery 
which  in  like  number  are  not  encountered  in  any  other  opera- 
tion. In  the  first  place  the  surgeon  is  dealing  not  only  with  the 
disease  for  which  he  is  operating,  but  there  may  be  many  com- 
plications not  directly  involved  in  the  malady  in  question.  In 
the  second  place,  particularly  in  toxic  goiters,  the  management 
of  the  patient  may  be  the  important  part  of  the  procedure.  This 
may  necessitate  a  variety  of  things  in  the  preliminary  treat- 

205 


206  DISEASES    OF    THE    THYROID    GLAXD 

ment,  but  during  tlie  course  of  the  operation  the  plan  may  need 
to  be  shifted  because  the  preoperative  estimate  of  the  patient's 
resistance  has  been  found  to  be  incorrect.  For  this  reason  it 
may  be  necessary  to  diagnose  the  case  as  the  operation  proceeds. 
No  more  may  be  done  than  the  patient  can  stand. 

The  Anesthetic 

TJie  choice  of  the  anesthetic  in  operations  for  goiters-  de- 
pends on  a  great  variety  of  factors.  Generally  speaking  but  two, 
ether  and  novocaine,  need  be  considered  though  a  few  surgeons 
employ  nitrous-oxide-oxygen  anesthesia.  With  the  last  named 
I  have  had  no  experience. 

Ether. — The  advantage  of  ether  is  chiefly  that  it  gives  the 
operator  a  free  hand.  He  does  not  need  to  consider  the  whims 
and  vagaries  of  the  patient.  He  can  work  without  any  annoy- 
ing consideration  as  to  the  ability  of  the  patient  to  stand  a  com- 
plete anesthesia  for  he  will  not  know  until  the  operation  is  com- 
pleted whether  or  not  she  can.  It  does  not  limit  the  surgeon  to 
any  refinement  of  technic.  If  he  spills  a  lot  of  blood  it  is  best 
that  the  patient  does  not  know  of  it. 

It  is  a  question  in  the  case  of  very  nervous  patients  who  in 
spite  of  every  care  in  preliminary  treatment  still  are  afraid  of 
the  operator  and  the  operation,  whether  the  shock  from  the 
fright  or  the  shock  from  the  anesthetic  will  be  the  greater.  If 
the  operator  by  his  personality  cannot  bring  the  patient  to  favor 
local  anesthesia,  or  accept  in  full  confidence  the  judgment  of  the 
operator,  ether  is  the  best  anesthetic.  The  only  alternative  is 
to  postpone  the  operation.  This  is  the  one  I  elect.  If  the  pa- 
tient cannot  be  calmed  for  the  local  anesthetic,  rest  and  seda- 
tives will  in  time  bring  about  such  a  state  of  tranquility  in 
nearly  every  case.  To  soak  a  frightened  patient  with  ether  is  to 
court  all  but  certain  disaster. 

Many  patients  stand  ether  very  well  and  the  beginner 
should  select  only  such  cases  as  will  take  ether  without  danger. 
He  then  is  free  to  consider  only  the  technic.  He  will  find  out 
later  whether  he  has  done  more  than  the  patient  can  stand. 

Against  ether  may  be  counted  the  increased  hyperemia  of 
the  field  of  operation  which  it  causes.  The  operation  is  more 
bloody  and  more  difiicult,  though  this  is  in  part  offset  by  the 


TECHXIC    OF    OPERATIONS  207 

freedom  the  surgeon  lias  in  that  it  is  possible  to  grab  anything 
in  any  way.  Packs  can  be  applied  with  a  degree  of  vigor  that 
the  patient  under  local  anesthesia  would  not  bear. 

The  patient  being  asleep,  interference  or  impending  com- 
pression of  the  trachea  are  not  recognized  early  and  disaster  is 
first  announced  by  the  asphyxiation  of  the  patient  demanding  a 
hasty  tracheotomy.  If  the  recurrent  laryngeal  nerve  is  endan- 
gered, the  surgeon  has  no  way  of  finding  out  until  the  patient 
salutes  him  the  next  morning  with  a  cracked-pot  voice.  The 
danger  of  pneumonia  is  greater  after  ether,  a  matter  of  great 
importance  in  old  patients  who  have  suffered  from  tracheal  ob- 
struction from  pressure  of  the  goiter. 

The  action  of  ether  on  the  hypertoxic  patient  may  be  open 
to  debate.  I  believe  the  resources  of  the  patient  are  tried  more 
b}^  the  general  anesthetic  than  b^^  the  nervous  tension  when  op- 
erated on  under  local  anesthesia.  I  use  ether  only  in  the  very 
young  and  the  obstreperous,  who  except  for  their  disposition, 
depart  but  little  from  the  normal,  that  is  to  say,  simple  colloid 
or  slightly  toxic  goiters. 

Novocaine. — This  drug  may  be  regarded  as  the  prototype 
of  all  local  anesthetics.  Other  chemicals  may  be  as  good;  to 
date,  none  is  better.  It  is  efficient  and  only  a  small  fraction  of 
the  amount  that  may  be  safely  administered  is  required  for  any 
goiter  operation.  The  question  of  safety,  therefore,  does  not 
enter.  It  is  efficient  because  complete  anesthesia  can  always  be 
secured.  The  sense  of  traction  or  compression  of  the  trachea  is 
all  that  can  appear  as  unpleasant  sensation  for  the  patient  to 
bear.  Usually  two  or  three  grains  of  novocaine,  with  5  to  8 
minims  of  epinephrine  to  the  ounce  makes  up  the  standard  solu- 
tion. From  one  to  two  ounces  of  the  solution  is  all  that  is  re- 
quired for  any  operation.  Four  times  this  amount  would  fall 
within  the  limits  of  safetj^  Highly  toxic  goiters  are  sensitive  to 
the  adrenaline  and  such  cases  may  require  the  lesser  amount  of 
epinex)hrine  while  very  vascular  goiters  make  the  larger  per- 
centage desirable. 

The  advantages  of  local  anesthesia  are  numerous.  It  makes 
a  bloodless  field  which  permits  exact  work  to  be  done.  This  not 
only  saves  blood  at  the  operation,  but  lessens  the  liability  of 
secondary  hemorrhage  because  the  vessels  are  accurately  caught 


208  DISEASES    OF    THE    THYHOID    GLA^D 

up  before  tliey  are  cut  and  tliey  can  be  then  accurately  and  se- 
curely ligated.  Impending-  compression  of  the  trachea  is  ob- 
served at  once  in  the  breathing  of  the  patient  and  the  gland  can 
be  so  manipulated  as  to  give  relief.  If  tlie  recurrent  laryngeal 
nerve  is  approached,  the  patient  at  once  responds  by  iri'itation 
of  the  larynx.  There  is  no  vomiting  after  operation  to  test  the 
efficiency  of  the  hemostasis.  The  ill-effects  of  the  anesthetic  on 
the  respiratory  tract  are  avoided.  The  excitement  incident  to 
the  administration  of  a  general  anesthetic  also  is  avoided.  Per- 
haps the  most  valua])le  feature  of  local  anesthesia  consists  in 
that  the  surgeon  can  gauge  the  type  and  extent  of  the  operation 
he  is  to  perform.  If  he  plans  a  lobectomy  but  discovers  that 
his  patient  shows  a  greater  degree  of  toxicity  than  he  had  an- 
ticipated, he  can  do  a  ligation  instead,  leaving  the  more  radical 
operation  for  some  future  sitting.  If  a  double  resection  seems 
more  than  the  patient  can  safely  stand,  one  lobe  only  can  be 
operated  on  leaving  the  other  for  a  future  sitting. 

The  disadvantages  of  local  anesthesia  are  that  the  operator 
must  plan  accurately  exactly  what  he  wants  to  do.  His  technic 
must  l)e  painstaking.  He  must  control  not  only  himself,  but  the 
patient  as  well.  The  whole  environment  nmst  be  regulated  so 
that  the  patient  is  not  undulj"  excited.  Local  anesthesia  is  not 
suited  for  the  inexperienced  goiter  operator  and  the  difficulties 
are  much  increased  if  the  operating  room  assistants  do  not  know 
how  to  comport  themselves. 

The  excitation  adrenaline  produces  in  very  toxic  patients 
nuist  be  considered  a  disadvantage.  The  excitement  incident  to 
the  adrenaline  subsides  in  from  ten  to  twenty  minutes  and  in 
nervous  patients  it  is  well  to  wait  until  it  does  subside. 

The  disadvantages  of  local  anesthesia  may  be  minimized  by 
developing  an  accurate,  gentle  technic.  Everything  pertaining 
to  the  operation  must  be  quiet  and  simple.  Noise,  loud  conver- 
sation and  the  like  nmst  be  prohibited. 

Anesthetization. — Inasmuch  as  a  general  anesthetic  is 
rarely  used  in  this  hospital,  the  following  description  of  technic 
presupposes  the  employment  of  local  anesthesia. 

The  most  important  factor  in  the  anesthesia  is  a  proper 
relation  between  patient  and  the  surgeon.  The  patient  must  feel 
assured  of  the  success  of  the  procedure.    If  the  patient  is  sent 


TECH  NIC    OF    OPERATIONS  209 

by  a  friend  wlio  lias  liad  an  operation  done  under  local  anes- 
thesia she  brings  this  attitude  with  her.  For  others  the  method 
of  approach  must  depend  on  the  personality  of  the  surgeon.  If 
one  is  an  expert  in  the  art  of  deception  it  may  be  an  advantage 
to  "steal"  the  gland.  If  one  is  not,  it  is  best  to  tell  the  patient 
simply  that  one  will  remove  a  part  of  the  gland  at  a  given  time 
or  whenever  she  is  in  proper  condition.  The  disadvantage  of 
stealing  the  gland  lies  in  that  the  patient  Avill  tell  her  friends 
that  she  did  not  know  when  she  was  to  be  operated  on  and  this 
second  patient  will  believe  every  manipulation  of  the  surgeon 
or  nurse  presages  the  operation.  Instead  of  the  strain  being  les- 
sened, it  Avill  be  multiplied  with  every  manipulation.  The  man 
M'ho  believes  he  is  stealing  anything  from  a  woman  is  only  fool- 
ing liimself. 

Before  beginning  the  anesthesia  it  is  desirable  that  the  pa- 
tient leceive  at  the  outset  a  good  impression.  She  should  be 
placed  on  the  operating  table  in  a  comfortable  position.  The 
surgeon  should  assure  himself  that  the  patient  is  relaxed,  con- 
tented and  satisfied  that  all  is  w^ell.  If  she  is  nervous  a  few 
words  of  encouragement  from  the  surgeon  may  allay  her  fears. 

The  Infiltration  of  the  Anesthetic. — The  gland  may  be 
gently  palpated  to  accustom  the  patient  to  the  pressure  of  the 
operator's  fingers.  The  initial  prick  of  the  needle  is  likely  to 
try  the  patient's  nerves  more  than  any  other  step  of  the  opera- 
tion. This  first  pain  can  be  materially  lessened  by  picking  up 
a  fold  of  the  skin  at  the  point  where  the  initial  puncture  is  to  be 
made  and  by  compressing  it  half  a  minute  between  the  thumb 
and  index  finger  cause  an  acute  anemia  (Fig.  80.)  The  prelim- 
inary prick  can  be  made  with  very  little  pain  at  the  point  of 
maximum  compression.  A  new  sharp  needle  causes  much  less 
pain  than  a  dull,  rusty  one.  The  initial  wheal  should  be  made 
slowly  lest  the  sudden  expansion  of  the  tissue  cause  pain. 

A  row  of  wheals  is  made  along  the  line  of  the  proposed  in- 
cision, this  being  usually  along  one  of  the  natural  folds  of  the 
skin  on  a  line  where  a  string  of  beads  would  naturally  fall  (Fig. 
81).  The  injection  must  be  made  endermically  which  is  in- 
dicated by  the  prompt  blanching  of  the  skin.  The  entire  extent 
of  the  proposed  incision  is  infiltrated  as  the  first  step  of  the 
operation.    If  the  solution  is  injected  below  the  skin,  anesthesia 


210 


DISEASES    OF    THE    THYROID    GLAXD 


is  not  instaiitaiieoiis  and  tlie  anesthesia  is  apt  to  disappear  be- 
fore the  time  for  suturing  the  skin  has  arrived.  After  the  skin 
has  been  infiltrated  the  platysma  should  be  infiltrated  by  pass- 
ing the  needle  parallel  with  the  skin  infiltration  but  deeply 
enough  to  reach  the  muscle. 


Fig.  80. — The  preliminary  needle  prick.  The  skin  is  pinched  firmly  between  the  fore- 
finger and  thumb  of  the  left  hand  as  the  needle  is  inserted.  Note  the  sterile  cap  made  by 
passing  a  drawstring  about  the  edge  of  a  loose  cap.  A  rubber  bathing  cap  covers  the  hair 
before   tlie   sterile   cap  is   put   on.      (Devised    by    Dr.    Chesky.) 


After  the  site  of  the  incision  has  been  anesthetized,  the  mus- 
cles of  the  neck  sliouhl  then  be  infiltrated.  The  sternomastoid 
and  the  stei  nohvoid  and  steriiothvi-oid  muscles  must  be  anesthe- 


TECHXIC    OF    OPERATIONS 


211 


tized.  These  muscles  receive  their  nerve  supply  from  the  hy- 
poglossal nerve,  a  different  source  than  the  skin  and  platysma. 
The  operator  can  readily  tell  when  his  needle  has  entered  the 
proper  i3lane  by  noting  when  the  needle  passes  through  the 


#% 


"A 


<Jr 


Fig.    81. — The    line    of    primary    infiltration.      A   line    of    wheals    is   made   just    above    the    sterno- 
clavicular   border.     The    infiltration    is    endermic. 


platysma  muscle.  By  moving  the  skin  and  platysma  one  can 
readily  prove  whether  the  needle  lies  in  the  proper  place.  Care 
should  he  taken  that  the  needle  does  not  pass  too  deeply,  thus 
wounding  the  sujjerficial  veins  of  the  gland  proper. 


212 


DISEASES    OF    THE    TKVUOII)    GLAND 


111  anesthetizing  the  imiseles  it  is  convenient  to  inject  the 
anesthetic  solution  in  the  muscle  covering  the  gland  over  the 
entire  site  of  the  operation.     This  not  only  assures  anesthesia 


Fig.  82.  -Intraiui;  cular  infiltration.  From  the  primary  line  of  infiltration  the  needle  is 
passed  between  the  platjsma  and  the  more  deeply  lying  muscles.  At  2  and  5  the  anterior 
cervical  and  the  supraclavicular  nerves  are  blocked.  At  4  and  .5  the  peritracheal  tissues  are 
infiltrated. 


but  facilitates  enucleation  by  producing  a  mild  edema  and  by 
constricting  the  small  vessels  everywhere  in  the  field  of  opera- 
tion. The  whole  area  can  be  reached  by  passing  the  needle 
throuch  the  original  line  of  infiltration.     The  mobilitv  of  the 


TECH  NIC    OF    OPERATIONS 


213 


skin  and  platysnia  make  it  possible  to  reach  every  part  of  tlie 
field  of  opei'ation  (Fi«>'.  82). 

It  is  likewise  advantageous  to  inject  deeply  about  the  poles 


/^ 


I 


i\ 


J 


/ 


fc  4 


y<^ 


4- 


'/ 


Fig  83.— Periglandular  infiltration.  The  needle  is  passed  between  the  gland  and  the  ovei- 
lying  muscles.  By  pressing  over  the  soft  parts  as  the  needle  is  being  passed  the  point  may 
be  made  to  reach  the  space  between  the  trachea  and  superior  pole  of  the  gland.  A  like 
maneuver  at  other  parts  of  the  gland  makes  it  possible  to  infiltrate  the  entire  periglandular 
tissue. 

of  the  gland  and  at  the  isthmus,  because  it  assures  anesthesia 
if  any  nerve  trunk  has  escaped  the  previous  infiltration.  It  also 
facilitates  enucleation.    By  depressing  the  needle  with  the  index 


214  DISEASES    OF    THE    THYROID   GLAND 

finger  of  tlie  left  hand  one  can  make  the  needle  follow  any  of 
the  planes  without  danger  of  injuring  any  of  the  neighboring 
structures  (Fig.  83). 

If  the  operator  desires,  the  needle  may  be  passed  over  the 
top  of  the  sternomastoid,  at  the  level  of  the  carotid  bifurcation, 
with  the  idea  of  blocking  the  cervical  nerves  at  the  point  where 
they  curve  over  that  muscle  {2  and  3,  Fig.  82).  If  it  succeeds  it 
but  anesthetizes  the  skin,  subcutaneous  tissue  and  platysma  but 
the  deeply  h^ing  muscles,  supplied  by  the  hypoglossal  nerves, 
are  not  influenced.  The  objection  to  the  blocking  of  the  cervical 
nerves  at  this  origin  as  a  means  of  anesthetizing  the  skin  area 
is  that  anesthesia  does  not  appear  at  once  and  the  vessel-con- 
stricting effect  at  the  site  of  operation  is  lost.  The  plan  above 
advised,  on  the  other  hand,  gives  instant  anesthesia,  is  unfailing 
in  its  results,  and  the  maximum  degree  of  constriction  of  the 
vessels  is  secured.  Besides  if  the  various  nerves  are  blocked  at 
their  roots  several  stabs  must  be  made  through  the  unanesthe- 
tized  skin. 

The  Skin  Incision 

The  injection  of  the  anesthetic  having  been  completed,  the 
incision  is  begun  at  once.  The  skin  is  incised  throughout  the 
entire  length  of  the  field  it  is  desired  to  expose.  The  initial  in- 
cision should  extend  through  the  skin  and  subcutaneous  tissue 
down  to  the  platysma  muscle.  This  skin  flap  is  dissected  up- 
ward off  the  platysma  for  the  distance  of  an  inch  or  two  (Fig. 
84).  This  is  done  in  order  that  the  platysma  may  be  incised  at  a 
higher  level  than  the  skin  incision.  This  gives  more  room  in 
which  to  find  the  anterior  jugular  veins  and  makes  a  careful 
coaptation  of  the  platysma  easy  in  the  closing  of  the  wound.  A 
few  oozing  points  may  be  encountered  at  this  stage.  These  are 
caught  up  and  ligated  at  once. 

Incision  of  the  Platysma 

The  platysma  is  then  incised  carefully  watching  for  the  an- 
terior jugular  veins  which  lie  beneath  the  fascia.  The  platysma 
is  dissected  up  from  the  fascia  to  permit  easj^  access  to  the  veins 
(Fig,  85).  The  extent  of  this  dissection  is  exaggerated  in  the 
figure  in  order  to  show  the  relation  of  the  veins  to  each  other. 


TECHXIC    OF    OPERATIONS 


215 


Four  are  shown  in  the  figure.  Usually  from  two  to  six  are  found. 
The  veins  after  being-  exposed  by  cutting  the  fascia  parallel  fo 
the  wall  of  the  vessels,  are  caught  up  between  two  forceps,  cut 
and  ligated  (Fig.  86).  The  ends  of  the  veins  should  be  under 
cut  (Fig.  86)  so  that  the  ligature  can  be  securely  placed.  If  this 
undercutting  is  not  done,  the  retracting-  vein  may  slip  its  lig- 
ature like  a  frightened  pup  slips  its  collar.  The  fascia  is  cut 
from  one  end  of  the  wound  to  the  other,  exposing  the  sterno- 
mastoid  muscles  and  the  short  muscles  covering  the  gland. 
When  the  fascia  is  cut,  it  retracts,  exposing  these  nmscles. 


Fig.  84. — The  preliminary  incision.  The  incision  is  made  along  the  line  of  the  primary 
infiltration  (Fig.  81)  down  to  the  platysma  muscle.  The  skin  and  subcutaneous  tissue  is 
then  dissected  off  from  the  platysma  so  that  the  incision  through  this  muscle  can  be  made 
at  a  higher   plane   than   the  skin   incision.      (Note  dotted  line.) 


Incision  of  the  Deep  Muscles  of  the  Neck 

The  sternohyoid  muscles  being  thus  exposed  are  divided 
from  the  edge  of  one  sternomastoid  to  the  other.  This  maneuver 
is  facilitated  by  picking  itp  the  muscle  with  tissue  forceps  (Fig. 
87).  By  doing  this  the  muscle  can  be  quickly  cut  Avith  a  knife 
without  endangering  the  vessels  of  the  thyroid  gland.  It  is  well 
to  separate  these  muscles  from  the  sternomastoid  muscles  for 
an  inch  or  more.  A  small  vessel  requiring  ligation  may  be  sev- 
ered in  this  procedure.     This  increases  the  space  sufficiently 


216 


DISEASES    OE    THE    TUVIIOID    ULAXI) 


without  tlie  necessity  of  incising  the  sternoniastoid  nuiscles. 
After  the  sternohyoid  muscles  are  cut  the  sternothyroid 
muscles  are  exposed.  The  gland  lies  just  below  these  muscles 
and  they  must  be  gently  lifted  from  the  gland  before  they  are 
cut.  When  there  has  been  much  reaction,  these  nuiscles  may  be 
quite  firmly  attached  to  the  gland  requiiing  care  in  their  separa- 
tion.   The  sternohyoid  muscles  are  incised  only  as  far  laterally 


Fig.  85. — Exposure  of  the  anterior  jugular  veins.  The  platysma  is  incised  along  the  line 
indicated  in  the  preceding  figure.  The  platysma  is  then  dissected  from  the  fascia  underneath. 
This  exposes  the  anterior  jugular  veins.  (The  area  exposed  is  double  that  ordinarily  per- 
formed in  order  to  show  the  venous  plexus  to  better  advantage.) 


as  is  needed  to  reach  the  outer  border  of  the  gland.  In  small 
glands  they  need   to  be  incised  but  little. 

In  some  instances  the  false  capsule  exists  as  a  separate 
plane  of  fascia  easily  separated  from  the  muscle  and  gland. 
AVlien  this  is  the  case  it  is  elevated  with  the  forceps  and  incised. 
Often  the  fascia  is  so  closely  attached  to  the  muscles  that  it  is 
elevated  and  cut  wdth  them. 

By  lifting  the  muscle  flap  so  mobilized,  additional  delicate 


TECHXIC    OF    OPERATIONS 


217 


planes  of  fibrous  tissue  covering  the  gland  may  be  identified  and 
all  above  the  true  capsule  must  be  lifted  upward.  By  so  doing, 
the  suspensory  ligament,  or  the  pyriform  lobe,  as  the  case  may 
be,  becomes  accessible  and  may  be  double  clamped,  ligated,  and 
divided  (Fig.  88).  This  step  is  important  because  a  small  ar- 
tery is  found  here,  too  small  to  bleed  much  when  cut  and  readily 
hidden  by  the  muscle  fiap  covering  it,  but  which  may  cause 
troublesome  late  hemorrhage.    By  dividing  the  suspensory  liga- 


Fig.  86. — Ligation  of  the  anterior  jugular  veins.  The  fascia  is  then  incised  parallel  to  the 
walls  of  the  veins  and  the  vessels  caught  between  two  forceps  and  the  vessel  is  cut  between 
them.  The  end  of  the  vessel  is  dissected  loose  for  a  quarter  of  an  inch  in  order  to  give  a 
better  hold   for  the  ligature. 

ment  so  early  in  the  operation  the  trachea,  as  far  as  the  isthmus, 
is  exposed  and  the  cleft  between  the  superior  pole  and  the  tra- 
chea is  made  more  accessible. 

Isolation  of  the  Superior  Pole 

Isolation  of  tlie  superior  pole  can  best  be  done  by  gently 
pushing  the  knife  handle  between  the  trachea  and  the  gland  tis- 


218 


DISEASES    OF    THE    THYROID   GLAND 


sue  (Fig.  89).  This  can  be  readily  done  without  danger  of  in- 
juring any  structure.  This  procedure  is  nuich  facilitated  if 
the  tissue  uniting  the  pole  to  the  trachea  was  edematized  during 
the  infiltration  of  the  anesthetic.  This  area  can  be  infiltrated 
after  the  gland  has  been  exposed  if  it  has  not  been  already  done. 
The  aid  in  separation  rendered  by  edematization  of  the  line  of 
separation  applies  to  all  other  borders  as  well.  If  the  tip  of  the 
lobe  extends  high  up,  it  may  be  drawn  downw^ard  by  grasping 


Fig.  87. — Incision  of  the  short  mviscles  covering  the  gland.  After  the  vessels  have  been 
tied  and  the  fascia  incised,  the  short  muscles  alone  cover  the  gland.  These  are  lifted  cfl 
from  the  gland  with  thumb   forceps  and   cut  with  a  knife. 


the  pole  with  forceps  and  making  gentle  traction  keeping  up 
meanwhile  the  manipulations  of  the  scalpel  handle.  The  outer 
surface  of  the  pole  is.  then  freed  from  adjacent  muscles  and  ves- 
sels. 

After  the  pole  is  dislocated  the  vessels  are  identified  either 
by  sight  or  palpation.  These  are  secured  by  passing  a  ligature 
about  them  or  about  the  extreme  upper  end  of  the  pole  of  the 
gland.    This  may  be  done  by  passing  a  threaded  needle  eye  end 


TECHNIC    OF    OPERATIONS 


219 


first  (Fig.  90)  or  by  lifting  up  the  pole  with  forceps,  grasping 
the  ligatures  and  pulling  them  under  the  pole  as  the  forceps  are 
withdrawn  (Insert  A,  Fig.  90).  The  separation  of  the  pole 
and  the  passing  of  the  ligature  is  much  facilitated  by  grasping 
the  gland  near  the  upper  pole  and  making  gentle  traction  down- 
ward as  the  pole  is  being  gradually  separated. 

If  the  vessels  are  much  displaced  by  the  irregular  develop- 


Fig.  88. — Ivigation  of  the  vessels  to  the  isthmus.  The  short  muscles  and  the  capsule  have 
been  incised  and  elevated  from  the  gland.  The  three  forceps  are  used  to  retract  the  muscieh 
and  capsule.  The  central  forceps  is  making  traction  on  the  suspensory  ligament.  A  suture- 
armed   needle   is  passed  around   the   ligament   securing   the   vessel. 


ment  of  the  gland  the  uppermost  point  may  not  represent  the 
pole  and  hence  the  vessels  may  be  missed.  The  vessels  should, 
therefore,  be  identified  by  sight  or  touch.  These  unusually  de- 
veloped lobes  sometimes  contain  small  vessels,  which  may  cause 
confusion  with  the  proper  vessels,  but  they  are  never  so  large  as 
a  normal  superior  thyroid  vessel.  (Compare  Fig.  77,  Chapter 
IX.) 


220 


DISEASES    OF    THE    THYROID   GLAliTD 


Separation  of  the  Lateral  Border  and  Ligation  of  the  Lateral 

Vessels 

The  superior  vessels  liaviiig  been  ligated,  tlie  lateral  surface 
of  the  gland  is  separated  by  means  of  the  handle  of  the  scalpel. 
Usually  it  is  easiest  to  separate  the  lateral  surface  down  to  the 
highest  point  of  its  concavity  and  then  proceed  to  a  partial  sep- 
aration of  the  lower  pole.    AVhen  the  lateral  wall  is  being  freed, 


^/>'0 


\w/s'//^  <,      


Fig  89. — Separation  of  the  superior  pole  from  the  trachea.  The  trachea  has  been  freed 
as  far  as  the  isthmus.  The  upper  pole  is  being  separated  from  the  trachea  with  the  handle  of 
the   scalpel. 


the  lateral  veins  should  be  sought  for.  If  the  field  is  free  from 
blood  these  veins  are  readily  identified  by  pulling  on  the  edges 
of  the  sternothyroid  muscles  at  the  lateral  end  of  the  incision. 
(See  Chapter  on  Anatomy.)  These  veins  should  be  double 
clamped  and  tied  (Fig.  91) ;  care  must  be  used  in  locating  these 
veins  for  they  are  thin  walled  and  are  easily  pulled  from  their 
union  with  the  internal  jugular  veins,  which  produces  a  very 
troublesome  hemorrhage.    Care  must  now  be  exercised  to  follow 


TECHNIC    OF    OPEPvATIOXS  221 

the  fascia  close  to  the  gland,  for  at  this  point  the  fascia  divides. 
By  following  close  to  the  gland  the  tissue  enclosing  the  parathy- 
roid glands  and  recurrent  nerves  can  be  avoided  even  if  it  is 
necessary  to  completely  dislocate  the  thyroid  gland  from  its  bed. 


Fig.  90. — Ligation  of  the  upper  pole.  The  upper  pole  has  been  freed  from  the  surround- 
ing tissue  and  a  suture-armed  needle  is  being  passed,  eye  end  first,  about  the  pole.  The 
gland  has  been  grasped  with  forceps  and  by  traction  the  pole  comes  into  the  wound.  The 
insert  shows  a  forceps  passed  under  the  pole  ready  to  grasp  a  ligature.  When  the  pole  is 
very   long   this   is   more   convenient   than   the    needle. 


Dislocation  of  the  Lower  Pole 

If  the  lower  lobe  is  not  large,  the  capsule  may  be  gently 
lifted  from  it  with  the  handle  of  the  scalpel.  If  this  lobe  ex- 
tends behind  the  clavicle,  traction  must  be  made  on  the  gland 
with  forceps  as  the  capsule  is  carefully  stripped  from  the  gland. 
Care  must  be  taken  lest  the  veins  be  torn. 

After  the  pole  has  been  dislocated  the  inferior  thyroid  ar- 
terv  is  located  in  the  lower  end  of  the  lateral  border.    The  ves- 


222 


diseasp:s  of  the  thyroid  gland 


sel  is  ligated  by  passing  a  needle  armed  with  a  siitnre  tliroiigli 
the  substance  of  the  gland,  in  such  a  way  that  the  artery  is  in- 
cluded (Fig.  92).  In  this  way  the  recurrent  nerve  is  most  surely 
avoided. 

Some  operators  advise  the  ligation  of  the  inferior  vessel 
at  some  distance  from  the  gland.  If  this  is  done  at  a  perfectly 
safe  distance  to  insure  safety  of  the  nerve,  the  incision  and  ex- 
posure is  unnecessarily  large.    If  one  ties  close  to  the  gland, 


Fig.    91. 


-Ligation    of    the    lateral    veins.       The    lateral    vein    has    been    grasped    between    two 
forceps  and   is   ready   for  section  and   ligation. 


the  nerve  may  be  caught  in  the  ligature  and  destroyed,  or  if 
the  tie  is  made  close  to  the  nerve,  the  distortion  may  disable  it 
temporarily  or  even  permanently,  even  though  the  nerve  is  not 
actually  included  within  the  ligature.  Furthermore,  the  poste- 
rior portion  of  the  gland  and  the  parathyroid  glands  secure  their 
nutrition  from  the  posterior  branch  and  if  the  main  trunk  is 
ligated  the  blood  supply  to  these  glands  may  be  endangered. 
Sometimes  small  branches  of  the   artery  may  be   discovered 


TECH  NIC    OF    OPERATIONS 


223 


Fig.  92. — Ligation  of  the  inferior  thyroid  artery  and  veins.  The  lower  pole  is  being 
pulled  upwards  with  forceps.  A  ligature  has  been  passed  about  the  lateral  branch  of  the 
inferior  thyroid  artery  at  the  left  of  the  figure.  At  the  bottom  a  ligature  has  been  passed 
about  the  veins  at  the  lower  pole. 


Fig.  93.— Topography  of  the  lateral  veins.  At  the  left  of  the  figure  forceps  are  making 
traction  on  the  capsule  of  the  gland.  The  forceps  on  the  right  are  making  traction  on  the 
gland  itself.     The  relation  of  gland  and  vein   thus  becomes  apparent. 


224  DISEASES    OF    THE    THYROID   GLAND 

higher  up  tlie  side  of  the  gland.  These  may  be  ligated  by  pass- 
ing a  needle  about  them. 

By  following  the  lower  jjole  medially  the  inferior  thyroidal 
veins  are  exposed.  These  are  secured  by  passing  a  ligature 
through  the  superficial  part  of  the  gland  (Fig.  92).  If  the  veins 
are  numerous  several  ligature-sutures  must  be  passed.  If  the 
thyroidea  ima  artery  is  present  it  should  be  ligated  separately. 

In  ligating  any  of  these  vessels  it  is  well  to  pass  the  ligature 
with  a  needle  in  such  a  way  as  to  include  a  portion  of  the  true 
capsule  of  the  gland;  this  prevents  the  ligature  from  slipping 
or  cutting  through  the  walls  of  the  vessels. 

Dislocation  of  the  Lobe 

The  lateral  vein  is  made  prominent  by  pulling  the  capsule 
lateralward  and  the  gland  medially  (Fig.  93).  After  the  lateral 
veins  have  been  clamped,  cut,  and  ligated,  the  lobe  is  dislocated 
by  gently  rolling  it  toward  the  trachea.  At  the  point  where  the 
median  vein  enters  the  gland,  the  fascia  divides.  The  one  plane 
follows  the  gland  toward  the  trachea,  passing  behind  the  para- 
thyroid glands  (Fig.  94).  The  other  plane  passes  outward  and 
is  lost  in  the  sternomastoid  sheath.  If  the  middle  vein  is  ig- 
nored and  the  separation  attempted  blindly  with  the  finger  (A, 
Fig.  94)  the  outer  plane  will  be  followed  and  the  operator  will 
attempt  to  lift  the  capsule  with  the  gland  together  with  the  par- 
athyroid glands  {B,  Fig.  94). 

If  the  middle  vein  is  tied  at  the  proper  time  and  the  gland 
is  properly  separated  from  its  false  capsule,  the  separation  need 
not  be  carried  so  far  as  to  endanger  the  parathyroid  glands  or 
the  recurrent  laryngeal  nerves.  This  relation  is  shown  in  Fig. 
95. 

Excision  of  the  Lobe 

After  the  superior  pole,  the  lateral  veins,  the  lateral  branch 
of  the  inferior  thyroid  artery,  when  it  can  be  located,  and  the 
inferior  thyroid  veins  have  been  ligated  and  the  gland  dislo- 
cated medially,  the  severing  of  the  gland  is  begun.  The  incision 
near  the  upper  pole  will  not  bleed  (Fig.  96)  because  these  ves- 
sels do  not  anastomose  with  the  inferior  vessels.  As  the  in- 
cision extends  downward,  small  bleeding  jjoints  may  be  found 


TECHNIC    OF    OPERATIONS 


225 


Fig.  94. — Wrong  method  of  managing  the  lateral  veins.  A,  The  finger  is  shown  separat- 
ing the  gland  from  its  capsule  without  preliminary  ligation  of  the  vein.  B,  The  finger  is 
shown  as  having  ruptured  the  vein  and  is  following  the  fascia  going  to  the  sheath  of  the 
vessels   instead    of   following   between    the   gland   and   capsule. 


226 


DISEASES    OF    THE    THYROID   GLAND 


Idferdlveia 
lasted   fi: 


^■<}\   '       Parathyroid'  '      ^IcS^^  Ju^uJarveii 


vein 
drt- 


Fig.  95. — Diagram  showing  the  appearance  after  the  resection  of  both  lobes.  The  lateral 
veins  have  been  ligated  and  the  remnant  of  the  lobe  separated  to  near  the  parathyroid  glands. 
The  topographic  relation  of  these  glands  is  not  disturbed.  Note  the  location  of  the  recur- 
rent  laryngeal    nerves. 


Fig.  96. — Resection  of  the  gland.  After  the  vessels  have  been  ligated  as  shown  in  Figs. 
90,  91,  and  92  the  gland  is  resected.  While  making  traction  downward  with  forceps  the 
gland  is  cut  below  the  ligature  about  the  upper  pole.  The  first  inch  of  the  incision  is  blood- 
less. 


TECHKIC    OF   OPERATION'S 


227 


anywhere  in  tlie  interior  of  the  gland.  Xoar  the  midportion  a 
short  distance  from  the  median  surface,  a  smart  bleeder  will  be 
invariably  encountered.  This  vessel  is  the  continuation  of  the 
posterior  branch  of  the  inferior  thyroid  artery  (Fig.  97).  By 
catching  up  the  bleeding  points  as  they  are  encountered,  the 
gland  can  be  rapidly  removed  without  any  considerable  loss  of 
blood. 


Branck  d. ; 
arfery  1, 


\ 


Fig.  97. — Completed  resection  of  the  right  lobe.  As  the  incision  from  the  point  shown 
in  Fig.  96  is  extended  downwards,  vessels  in  the  substance  in  the  gland  are  encountered. 
These  are  caught  up  and  are  shown  ligated.  Two  staple  sutures  approximate  the  cut  edges. 
The  upper  has  been  tied,  the  lower  passed  but   not  tied. 


The  bleeding  points  above  mentioned  are  ligated  by  stitch- 
ing around  them  through  the  stump  of  the  gland  with  a  needle 
(Fig.  97).  An  ordinary  ligature  should  not  be  trusted  because 
the  vessels  tend  to  retract  and  may  slip  a  ligature  unless  it  is 
secured  by  passing  it  into  the  gland  tissues  as  above  indicated. 

In  toxic  goiters  the  gland  is  so  fragile  that  hemostasis  may 
be  secured  with  difficulty.     Mass  ligatures,  taking  in  as  much 


228  DISEASES   OF   THE   THYROID   GLAND 

as  possible  of  the  gland,  are  usually  successful.  These  may  be 
passed  from  one  capsule  to  the  other,  bringing  one  edge  of  the 
gland  toward  the  other  as  much  as  possible  (Fig.  97).  In  these 
cases  the  problem  of  hemostasis  is  the  same  as  that  in  wounds 
of  the  liver.  I  have  not  found  open  packing  of  the  wound  neces- 
sary or  the  suturing  of  the  muscle  stump  to  the  cut  surface. 
Neither  have  I  found  the  leaving  on  of  clamps,  as  recently  rec- 


Fig.  98. — The  folding  downwards  of  ihe  upper  pole.  The  cut  edge  of  the  upper  pole  is 
folded  downwards  by  means  of  a  staple  suture.  A  suture  is  passed  through  the  lower  pole 
but  has  not  been  tied. 

ommended  by  Bartlett,  necessary.  At  the  same  time,  I  should 
not  hesitate  to  employ  any  of  these  means  should  occasion  arise. 
I  did  find  it  necessary  once  to  pack  because  of  tearing  off  the 
lateral  vein  during  the  stage  of  enucleation.  Both  patient  and 
operator  recovered  in  two  days  and  the  operation  was  success- 
fully completed.  It  is  well  for  the  young  surgeon  to  remember 
that  should  alarming  hemorrhage  occur  packing  may  be  re- 
sorted to,  and  if  need  be,  the  completion  of  the  operation  de- 


TECTTNIC    OF    OPERATIONS  229 

ferrecl  to  a  later  date.     I  would  again  elect  anything  in  pref- 
erence to  death  from  hemorrhage  on  the  table. 

Disposal  of  the  Pole  Stumps 

When  all  bleeding  points  have  been  secured,  ligatures  are 
passed  through  the  stump  of  the  superior  pole  and  through  the 
body  of  the  gland  (Fig.  98).  The  stump  of  the  inferior  pole  is 
pulled  ui)ward  in  like  manner  (Fig.  99).  This  brings  these  cut 
ends  to  lie  on  the  cut  surface  of  the  body  of  the  gland  and  pre- 
vents the  muscle  and  fascia  from  adhering  to  the  underlying- 
gland.  This  technic  exposes  a  smoother  surface  over  which  to 
unite  the  capsule  and  it  shortens  the  long  axis  of  the  gland  to 
more  nearly  that  of  the  normal  gland. 

Management  of  the  Second  Lobe 

The  next  step  depends  on  the  amount  of  tissue  the  operator 
deems  it  desirable  or  safe  to  remove.  The  operation  may  be 
terminated  at  this  point  or  one  of  two  courses  may  be  pursued. 
If  the  major  portion  of  the  opposite  lobe  is  to  be  removed,  the 
technic  just  described  inaj  be  carried  out  on  the  other  side  also. 
If  the  removal  of  less  gland  tissue  is  deemed  sufficient,  a  partial 
resection  may  be  done.  It  is  probably  true,  as  many  surgeons 
believe,  that  the  more  tissue  removed  the  surer  the  results. 
However,  we  do  not  as  yet  know  the  end  results  of  such  radical 
procedures.  Hence  I  frequently  elect  to  obliterate  only  a  part  of 
the  lesser  lobe,  leaving  enough  to  insure  an  unimpaired  circula- 
tion in  the  least  affected  lobe. 

When  it  is  desirable  to  destroy  but  a  part  of  the  lobe  a  V- 
sliaped  piece  of  the  gland  is  removed.  This  is  done  by  passing 
a  ligature  deeply  through  the  gland  some  distance  from  the 
lower  pole  (Fig.  99).  A  like  suture  is  passed  through  the  gland 
near  the  upper  pole.  Any  amount  of  tissue  may  be  removed 
depending  on  where  these  mass  ligatures  are  placed.  A  large 
V  is  then  cut  from  the  gland  between  these  ligatures  (Fig.  100). 
The  cut  surfaces  thus  remaining  are  approximated  by  sutures 
(Fig.  101).  In  very  fragile  glands,  as  in  very  toxic  goiters,  this 
method  is  not  suited  because  of  the  tendency  of  the  ligatures  to 
cut  through  the  soft  tissue.     In  such  cases  the  operator  had 


230 


DISEASES    OF    THE    THYROID   GLAND 


better  be  satisfied  with  the  removal  of  the  major  part  of  one 
lobe. 

Closure  of  the  Wound 

The  operation  is  now  completed  and  the  wound  is  ready  for 
closure  (Fig.  101).  When  the  capsule  has  been  separated  from 
the  sternothyroid  muscle,  it  may  be  closed  separately  over  the 


Fig.  99. — The  folding  of  the  poles  completed;  resection  of  the  remaining  lobe.  The  folding 
in  of  the  lower  pole  is  shown  completed  by  the  tying  of  the  suture  noted  in  the  preceding 
figure.  A  wedge  resection  of  the  opposite  lobe  is  begun  by  ligating  en  masse  near  the  upper 
pole.     The   needle  is   being  passed  through  the   gland   near  the   lower  pole. 

gland.  Often  it  makes  up  the  posterior  sheath  of  these  muscles. 
In  this  event  the  muscle  is  pulled  over  the  cut  surface  of  the 
gland  and  united  in  a  longitudinal  line  (Fig.  102). 

The  ends  of  the  sternohyoid  muscles  are  then  identified  and 
brought  into  apposition.  When  the  operation  is  done  under 
local  anesthesia,  it  is  rarely  that  bleeding  vessels  are  encoun- 
tered in  the  muscle  stumps.  If  such  should  be  encountered 
they    are    caught  with  a  clamp   and   when  the  muscle   ends 


TECHNIC    OF    OPERATIONS 


231 


are  coapted  a  figure-of-eight  suture  is  used.  If  there  has  been 
no  bleeding,  a  simple  running  suture  or  staple  suture  may  be 
used  and  is  preferable  because  it  causes  less  rolling  up  of  the 
ends  of  the  muscles  (Fig.  103).  Care  should  be  exercised  to 
bring  the  muscle  ends  in  good  coaptation.  The  lateral  border 
of  the  sternohvoid  muscles  are  then  sutured  to  the  medial  bor- 


Fig.   100. — Wedge  resection  of  the  opposite  lobe.     The  ligatures  mentioned   in  the  preceding 
figure   have   been    tied   and   the   wedge   of    tissue    is   being   excised. 


ders  of  the  sternomastoid  muscles  in  order  to  obliterate  any 
dead  spaces  at  this  point. 

The  platysma  is  then  united  throughout  its  extent  by  a  run- 
ning suture  (Fig.  104).  A  careful  coaptation  of  this  muscle  does 
much  to  prevent  attachment  of  this  line  of  sutures  to  the  deeper 
structures  of  the  neck.  If  this  is  not  done  the  platysma  may 
become  adherent  to  the  deeper  structures  and  the  skin  will  make 
excursions  with  the  trachea  in  deglutition.  This  annoys  the  pa- 
tient and  brings  chagrin  to  the  surgeon. 


[O^cM^j 


/*!?/// 


Fig.    101.— The    resection    completed.      The    wedge    excision    shown    in    the    preceding    figure 
has  been  completed  and  the  cut  surfaces  ccapted  by  sutures. 


Fig.  102. — The  closure  of  the  capsule.  The  operation  having  been  completed  as  in  the 
preceding  figure  the  false  capsule  is  closed  over  the  stumps  of  the  lobes.  If  the  tibrous 
capsule  is  identified  it  may  be  used.  If  not  the  borders  of  the  sternothyroid  muscles  are 
brought  together. 


TECHXIC   OF   OPEBAXIOSTS 


233 


Usually  after  the  platysma  has  been  united,  there  remains 
the  gapping  snbcntaneons  fat.  The  extent  of  this  is  dejjendent 
on  the  adiposity  of  the  patient.  In  thin  subjects,  particularly  in 
old  women,  it  may  be  neglected,  but  in  plump  ones,  especially 
when  a  fine  scar  is  desired,  a  subcutaneous  layer  of  sutures 
should  be  passed  (Fig.  1(^).  This  is  done  with  a  straight  sharp 
needle. 

If  the  subcutaneous  sutures  have  been  properly  placed. 


/      \ 


Tig.  103. — ^The  restoration  of  the  stcsnohjoid  Bmascles^  Tlbe  cm  ends  of  the  mnseks  aie 
identified  and  coapted  either  by  a  stcapk  snture  or  by  a  figur«H>f-«ia^t  sotnrt  If  there  is 
an  erersioa  of  the  edges  these  may  be  nnitcd  by  secondary  satnre& 

little  is  neeiled  to  eoapt  the  skin.  The  finest  available  suture  is 
desired.  Hoi-se  hair  is  perhaps  the  best  material  available.  A 
staple  suture  is  used  in  order  that  the  epidennal  layer  may  be 
brought  into  more  accurate  coaptation  (Fig.  106). 

Sutures  Used 

Pyoetanin  Xo.  2  is  used  for  ligation  of  the  poles.  Pyoctanin 
Xo.  0  for  all  other  ligatures  and  sutui-es.  Hoi-se  hair  or  '*dermal 
suture''  is  used  in  the  skin. 


234 


DISEASES    OF    THE    THYROID   GLAND 


Fig.    104. — The    coaptation    of    the    platysma    muscle.      The    cut    edges    of   the    platysma    muscle 
are  brought  together  with  a  running  suture. 


Fig.  105. — The  coaptation  of  the  subcutaneous  fat.  After  the  platysma  muscle  has  been 
united  a  subcutaneous  suture  is  placed  in  the  fat  so  that  the  edges  of  the  skin  fall  together. 
The  suture  likewise  obliterates  the  dead  space.     This  is  important  in  fat  patients. 


TECHNIC    OF    OPEEATIONS 


235 


^yA^ 


Fig.  106. — The  closure  of  the  skin.  After  the  edges  have  been  brought  together  by  the 
subcutaneous  suture  the  edges  of  the  skin  are  brought  into  exact  apposition  by  staple  sutures 
of  horse  hair. 


236  DISEASES    OF    THE    THYROID   GLAND 

Drainage 

Drainage  is  not  used  except  in  special  cases.  If  one  elects 
to  close  without  drainage  the  surgeon  must  be  sure  of  his 
liemostasis.  The  beginner  had  better  drain.  In  very  fragile 
glands  where  the  liemostasis  is  not  satisfactory,  a  gauze  drain 
is  used,  the  end  being  passed  down  to  the  offending  surface. 
This  performs  the  double  purpose  of  aiding  coagulation,  should 
hemorrhage  occur,  and  it  permits  the  blood  to  escape  from  the 
wound  should  there  be  considerable  bleeding.  In  large  intra- 
thoracic goiters,  where  a  cavity  is  unavoidably  left,  drainage  is 
alw^ays  placed.  Here  a  rubber  tube  is  preferable  to  gauze,  for 
it  is  desirable  that  any  hemorrhage  that  may  occur  be  at  once . 
conducted  to  the  surface.  In  the  substernal  lobes,  the  capsule 
can  be  drawn  up  and  the  cavity  obliterated,  thus  obviating  the 
need  for  drainage.  In  old  women  and  men  where  scarring  is  of 
minor  importance,  drainage  may  be  placed  with  less  hesitation 
than  in  persons  in  whom  a  tine  scar  is  desirable. 

Pole  Ligation 

In  patients  too  toxic  to  permit  lobectomy,  ligation  of  one  or 
more  vessels  may  be  resorted  to.  In  vascular  goiters  this  seems 
sometimes  beneficial.  At  any  rate  it  assures  rest  in  bed  and  it 
is  a  rehearsal  for  the  patient  for  the  main  operation  to  come,  and 
it  gives  the  surgeon  a  means  of  judging  the  patient's  reaction  to 
operation.  The  reason  so  little  is  to  be  expected  from  superior 
pole  ligation  is  that  the  superior  thyroid  artery  supplies  but  a 
small  part  of  the  gland  and  the  blood  supply  of  the  greater 
portion  is  not  materially  influenced. 

Some  operators  have  recommended  the  ligation  of  all  four 
of  the  principal  arteries.  This  is  quite  a  serious  undertaking, 
quite  as  serious  as  lobectomy.  I  fear  to  do  this  lest  too  great  a 
part  of  the  circulation  be  cut  off  thus  not  only  endangering  the 
remaining  part  of  the  thyroid  gland,  but  the  parathyroid  bodies 
as  well.  I  fear  it  because  I  have  seen  conditions  years  after 
operation  which  I  did  not  understand  and  the  possibility  of  too 
great  a  part  of  the  gland  being  deprived  of  its  blood  supply 
seems  a  possibility. 

Tlie  ligation  of  tlie  superior  poles  is  a  relatively  harmless 


TECHNIC    OF    OPERATIONS  237 

procedure  and  may  be  done  in  tlie  liope  tliat  it  may  do  some 
good.  It  should  not  be  forgotten,  however,  that  death  has  fol- 
loAved  pole  ligation  and  even  in  this  simple  operation  the 
grounds  should  be  carefully  considered.  Pronounced  rise  of 
temperature,  extreme  emaciation,  and  delirium  are  the  symp- 
toms that  contraindicate  it.  Pole  ligation  is  most  apt  to  be  of 
benefit  in  large,  soft  glands  which  show  expansile  pulsation;  in 
such  cases  ligation  sometimes  produces  brilliant  results. 

The  technic  is  relatively  simple.  A  line  tw^o  inches  long  is 
anesthetized  along  one  of  the  wrinkles  of  the  skin  nearest  the 
superior  pole.  The  platysma  and  the  deeper  muscles  are  then 
infiltrated.  Next  the  tissue  about  the  pole  is  abundantly  infil- 
trated both  to  secure  the  anesthesia  and  anemia  but  also  to 
facilitate  dissection.  The  skin,  subcutaneous  fascia,  and 
platysma  are  then  incised  throughout  the  length  of  the  infil- 
trated line.  The  pole  is  then  palpate-d,  and  the  deeply  lying 
muscles  are  split  and  retracted.  The  vessel  can  now  usually  be 
palpated.  It  is  further  freed  until  its  pulsations  can  be  seen.  A 
silk  thread  is  then  passed  around  the  vessels  and  tightly  tied. 
If  one  elects  the  upper  end  of  the  pole  may  be  ligated  instead  of 
the  artery  and  veins.  I  do  not  ligate  the  inferior  thyroid  ar- 
teries. The  results  obtained  do  not  w^arrant  an  operation  of 
such  magnitude,  in  my  judgment. 


INDEX 


Abdoniiiial  dropsies,  105 
Aberrant  goiters,  88,  149 

locations  of  thyroid  arteries,  201 
tumors    of   the    submaxillary   region, 
151 
Accessory  thyroid  glands,  149 
Acidosis,  postoperative,  169 
Acinal  cells  of  exophthalmic  goiter,  69 
Acini  of  thyroid  gland,  34 
Adenoma,  diffuse,  60 

fetal,  59,  61 
Adenomatous  goiter,  58,  59 
diffuse,  64 
glandular  type,  65 
papillary  type,   66 
Adolescent  colloid  goiter,  prognosis  in, 
126 
goiter,  diagnosis  of,  112 
treatment  of,  176 
Adrenaline,  in  goiter  operations,  208 

test,  109 
Age  in  relation  to  goiter,  17 
Amenorrhea  in  toxic  goiter  cases,  20 
Anatomy,  of  thyroid  gland,  normal  and 

pathological,  28 
Anemia  in  goiter,  105 
Anesthesia,    intramuscular    infiltration, 
212 
periglandular  infiltration,  213 
Anesthetic,  infiltration  of,  209 

in  goiter  operation,  206 
Anesthetization,   in    goiter    operations, 

208 
Appetite,   102 

Arteries  of  the  thyroid  gland,  196 
Artery   to    suspensory   ligament,   196 
A«i)liyxiation  in    goiter    operation    un- 
der ether,  207 
AtA'pical  forms  of  goiter,  diagnosis  of, 
119 


B 

Basal  metal)olism,  in  goiter,  110 

Basedow  heart,  123 

Basedow's  disease,  121 

Blood  changes  in  goiter,  105 
pressure  in  goiter  cases,  97 
supply  of  the  thyroid  gland,  194 
vessels  of  the  thyroid  gland,  32 

Eoue   formation  within  colloid  goiters, 
56 


Brain  hemorrhages  in  goiter,  79 
Bronchitis,  postoperative,   172 


Calcareous  areas  in  colloid  goiters,  47 

degeneration   in   colloid  goiter,   55 
Carcinomatous    degeneration   in   colloid 

goiter,   57 
Carotid  tumors,  152 
Capsule,    closure    of,    232 
false,  190 
morphology  of,  28 
Circulatory  apparatus,  pathology  of,  in 

goiter,  83 
Coagulation  time,  changes  iai,  108 
Collapse  of  the  trachea,  postoperative, 

166 
Colloid  goiter,  37,  42 

bone  formation  within,  56 
calcareous  degeneration  in,  47,  55 
carcinomatous  degeneration  in,  57 
cystic  degeneration  in,  51 
degeneration  with   secondary   hem- 
orrhages in,  45 
diagnosis  of,  112 
early  operative   treatment,   180 
endemic,  44 
fetal  adenoma  in,   61 
fibrous  degeneration  in,  46 
tissue  degeneration  in,  54 
gross  pathology,  45 
histology  of,  48 
hyaline   degeneration  in,  57 
in  adult,  prognosis  in,  127 

treatment  of,  179 
malignant  degeneration,  58 
myocardial  changes  in,  50 
operative  treatment,  179 
prognosis  in,  126 
resting,  44 

secondary  changes,  51 
substance  in  toxic  goiter,  73 
Complications,  postoperative,  166 
Compression  of  trachea  by  goiter,  134, 

135 
Congenital  goiters,  17 
Consistency  of  thyroid  gland  in  goiter, 

87 
Constipation  in  goiter,  103 

management   of,  in  toxic  goiter,  160 
Cough,    constant,    as    symptom  of  ab- 
normally situated  goiter,  143 


239 


240 


INDEX 


Cystic   clcjjoiicratioii   in   colloid  goiters 

51 
Cysts  of  the  thyroid,  53 

D 

Degeneration,  mass,  with  lieniorrliage  in 
colloid  goiter,  48 
secondary,  prognosis  in,  129 
Degenerative  toxic  goiter,   71 
Diagnosis     of     abnormal     location     of 
goiter,  138 
of   abnormally   situated   goiter,   143 
of  thyroid  disease,   112 
Diarrhea  and  vomiting  in  toxic  goiter, 
160 
in  goiter,  102 
Diet  in  preoperative  treatment  of  toxic 
goiter,  158 
postoperative,  166 
Diffuse  adenoma,  60 

adenomatous  goiters,   63 
Digestive  disturbances,   102 

tract,   pathology   of,   in   goiter,   83 
Drainage,  236 
Drugs    in    preoperative    treatment    of 

toxic  goiter,  159 
Dysphasia  in  goiter,  136 
Dyspnea    as    symptom    of    abnormally 
situated  goiter,  142 

E 

Endemic  goiter,  usually  colloid  type,  44 
Endemiology,  21 
Ether  in  goiter  operation,   206 
Etiology    and    pathogenesis    of    goiter, 

17 
Exophthalmia,  in  goiter,  89 
Exophthalmic  goiter,  nervous  trauma  in 
etiology  of,  24 
papillary  formation  in,  67 
Eye  signs  in  pupillary  type  of  adenom- 
atous goiter,  66 
Graefes'  sign,  91 
Mobius'   sign,    93 
symptoms,     disturbance     in     conver- 
gence,  92 
Gifford's  sign,  93 
imperfect  movement  of  upper  lid, 

90 
in  goiter,  88 
nystagmus,  93 
pupil  sign,  93 
tear  secretion,  93 


F'alse  capsule,  190 
Fetal  adenoma,  59,  61 
in  colloid  goiter,  61 
adenomas,  prognosis  in,  128 


Fibrous   tissue   degeneration   in   colloid 

goiter,  54 
Forme  fruste,  diagnosis  of,  120 

differentiation    from    Graves'    dis- 
ease,  121 

goiters,   76 

interstitial  treatment  of,  183 

ovarian  hypoplasia  associated  with, 
122 

pelvic  organs  in  relation  to,  19 

prognosis  in,   130 

rapid    heart    most   constant   symp- 
tom, 123 

G 

Genital  disturbances  in  goiter  cases,  19 

lesions     associated     with     secondary 
toxic   goiter,   118 

tract,  pathology   of,   in   goiter,   82 
Gifford's  sign,  93 
Glandular   degeneration,    71 

proliferations,  63 

type  of  adenomatous  goiter,  05 
Goetsch  test,   108 
Goiter,  aberrant,  88,  149 

abnormally    situated,     diagnosis    of, 
143 
symptoms,  142 

acidosis  postoperative,  169 

adenomatous,  59 

adolescent,  diagnosis  of,  112 
treatment  of,  176 

adrenaline  test,  109 

age  in  relation  to,  17 

amenorrhea  in  cases  of,  20 

anemia  in,  105 

appetite  in,  102 

at>-pical  forms,  diagnosis  of,   119 

basal  metabolism  in,  110 

blood    changes    in,    105 
pressure  in,  97 

brain  hemorrhages  in,  80 

bronchitis  postoperative,  172 

care  of  wound,  164 

changes  in  coagulation  time,  108 

circulatory   apparatus,   pathology   in, 
83 

classification   of   pathology   of,   41 

collapse  of  trachea,  postoperative, 
166 

colloid,  43   {see  colloid  goiter) 

compression  of  trachea  by,  135 

consistency  of,   87 

constipation  in,  103 

degenerative  toxic,  71 

degree  of  thyroid  enlargement,  85 

diagnosis  of,  112 

abnormal  location  of,  138 

diarrhea  in,  102 

diet    in    preoperative    treatment    of, 
158 


INDEX 


241 


Goiter — Cont  'd. 

diet,   postoperative,   166 
digestive  disturbances,   102 
digestive  tract,  pathology  in,  S3 
drugs   in   preoperative   treatment   of. 

159 
dysphasia  in,  136 
endemiology  of,   21 
etiology  and  pathogenesis   of,   17 
examination  for,  86 
exophthalmia  in,  89 
eye  symptoms  in,  88 
genital     disturbances    accompanying, 

19 
genital  tract,  pathology  in,  82 
glandular  degeneration,  71 
Goetsch  test,  108 
Graefe's  sign,  91 
heart  in,  95,  99,  116 

postoperative  care  of,  165 
hemorrliage   postoperative,   167 
heredity  as  factor  in,  20 
hoarseness  postoperative,  168 
hyperacute    forms    of,    diagnosis    of, 

119 
hypophysis  pathology  in,  82 
icterus  in,  103 
in  pigs,  22 

infectious  theory  of,  22 
intestinal  hemorrhages,  104 

proliferative,   76 
iodine  in  prevention  of,  22 
kidney  pathology  in,  83 
laryngitis,  postoperative,  163 
leucocytosis  in,  106 
lingual,  150 
liver  pathology  in,  83 
malignant  degeneration,  diagnosis  of, 

114 
management  of  constipation   in   pre- 
operative treatment,  160 
mania  in  hyperacute  forms,  119 
muscular  fatigue  as  symptom  of,  94 

system  in,  83 
myxedema   postoperative,    173 
nerve  compression  in,  136 
nervous  shock  in  etiology  of,  24 

system,  pathology  in,  79 
nervousness  postoperative,   162 
neurogenic  theories,  23 
nontoxic,  preoperative  treatment,  156 
nursing  care,  postoperative,   161     ' 
operation,   anesthetic,   206 

anesthetization,  208 

closure  of  wound,  230 

complications,   205 

dislocation  of  lower  pole,  221 
of  the  lobe,  224 

disposal  of  pole  stumps,  229 

drainage,   236 

ether  in,  206 


Goiter,  operation — .Cont  'd. 

excision  of  lobe,  224 

hemostasis  in,  205 

incision    of    deep    muscles    o±  the 
neck,   215 
of   the  platysma,   214 

infiltration  of  anesthetic  in,  209 

intramuscular  infiltration,  212 

isolation  of  superior  pole,  217 

jugular  veins  exposed,  216 

ligation  of  lateral  veins,  222 

local  anesthesia  in,  207 

management    of     bleeding    points, 
227 

mortality  after,   131 

novocaine  in,  207 

periglandular  infiltration,  213 

pole  ligation,  236 

resection  of  gland,  226 

second  lobe,  management  of,  229 

separation    of   lateral    border    and 
ligation  of  lateral  vessels,  220 

skin  closure,  235 

skin   incision,   214 

sutures  used,   233 

time  of  in  toxic  goiter,  160 
operations,  adrenaline   in,   208 
operative  mortality,  131 
osseous  system  in,  84 
pain,  postoperative,  162 
pancreas  pathology  in,  82 
parathyroid  pathology  of,  82 
pathology  of  other  organs  associated 

with,  79 
patients,     hospital    management     of, 
156 

instructions  at  dismissal,  174 
pituitary  disturbances  in,  20 
pneumonia  postoperative,   172 
postoperative  complications,   166 

treatment,  161 
previous  and  associated  diseases,  23 
primary  toxic,  treatment  of,  181 
prognosis  of,  125 
rest  in  treatment  of,  157 
scars   following   operation,   171 
secondary  adenomatous,  74 

toxic,  71 

diagnosis  of,  117 

genital    lesions    associated    with, 

118 
treatment  of,   181 

toxicity,  diagnosis  of,  114 
sensitiveness  of,  88 
sex  in  relation  to,  18 
shock  postoperative,  169 
size  and  rapidity  of  growth,  87 
skin   changes   in,   104 
substernal  and  intrathoracic,  138 
suprarenal  gland  pathology  in,  82 
symptomatology  of,  85 


242 


INDEX 


Goiter— Cont  'd. 
tachycardia  in,  9(5 
temperature,     postoperative     control 

of,  162 
tetany  postoperative,  172 
thvanus   pathology   in,   80 
thyrogenic  tlieory,  25 
time  of  operation,  160 
toxemia,  postoperative,  163 
toxic   {see  also  toxic  goiter) 
diagnosis  of,   116 
differentiation  of,   from  tuberculo- 
sis, 117 
preoperative  treatment  of,  156 
prognosis  in,  128 
tracheitis  postoperative,  163 
treatment  of,  175 
tremor  in,  94 
vomiting  in,  102 

and   diarrhea   in,   160 
postoperative,  161 
wandering,  140 
x-ray  examination,  86 
unusual   locations,    133 
Goose    cough    in    abnormally    situated 

goiter,  143 
Graefe's  sign,  91 

Graves'     disease,     relation     of      forme 
fruste  to,  121 

H 

Laryngeal  nerves,  recurrent,  193 
postoperative  treatment,  165 
rapid,  as  constant  symptom  of  forme 

fruste,  123 
sounds  in  goiter,  99 
thyrotoxic,   100 
Hemorrhage  into  substernal  goiter,  145 
management  of,  in  goiter  operation, 

227 
postoperative,  167 
Hemorrhages,  brain,   in  goiter,   80 

in  colloid  goiters,  47 
Hemostasis  in  goiter  operation,  205 
Heredity  as  factor  in  goiter,  20 
Histology  of  colloid  goiter,  48 
Hoarseness,  postoperative,  168 
Hospital    management    of    goiter    pa- 
tients, 156 
Hyaline  degeneration  in  colloid  goiter, 

57 
Hyperacute  fomis  of  goiter,  diagnosis 

of,  119 
Hvpertoxic  patient,  effect  of  ether  on, 

207 
Hypophysis,  pathology  of,  in  goiter,  82 


Icterus,  s\"mptom  of  goiter,  103 
Infection   following   operation,    170 


Infectious  theory  of  goiter,  22 
Inferior  thyroid  arteries,  198 
Infiltration  of  anesthetic,  209 
Instructions  to   goiter  patients  at  dis- 
missal, 174 
Interacinal  cells  in  thyroid  gland,  37 
Interstitial  proliferative  goiters,  76 
Intestinal  hemorrhages,  as  symptom  of 

goiter,  104 
Intramuscular  infiltration,  212 
Intrathoracic  goiter,  138 

diagnosis  of,   144 

treatment,  147 
struma,  152 

diagnosis,  153 

symptoms,  153 

treatment,  155 
Iodine  in  prevention  of  goiter,  22 


Jugular  veins,  exposure  of,  in  goiter  op- 
eration, 216 
ligation  of,  in  goiter  operation,  217 

K 

Kidneys,  pathology  of,  in  goiter,  83 
Kindness  in  preoperative  treatment  of 
toxic   goiter,   157 


Laryngeal  nerves,  recurrent,  193 

superior,  193 
Laryngitis,  postoperativej  163 
Leucocytosis  in  goiter,  106 
Levator  glandulae   thjToideae,  188 
Ligation  of  jugular  veins,  217 
of  upper  pole,  221 
of  vessels,  typical  sites  of,  202 
Limestone     associated     with     endemic 

goiter,  21 
Lingual   goiter,   150 
treatment,  151 
goiters,  diagnosis,  151 

differentiation  from  dermoids,  151 
symptoms,  150 
Liver,  pathology  of,  in  goiter,  83 
Lobe,  dislocation  of,  in  goiter    opera- 
tion,  224 
excision  of,  in  goiter  operation,  224 
Local  anesthesia  in  goiter  operation,  ad- 
vantages of,  207 
Lower  pole,  dislocation  of,  221 
Lungs,  involvement  of,  in  goiter,  115 
Lymph  vessels  of  the  thyroid  gland,  34 

M 

Malignancy  in  substernal  goiter,  143 
in  intrathoracic  goiter,  145 
prognosis  in,  131 


INDEX 


243 


Malignant    degeneration,    diagnosis    of, 
114 
in   colloid   goiter,    58 
Mechanical  goiter  heait,  100 
Mediastinal  tumor,  146 
Medical  treatment  of  adolescent  goiters, 

177 
Menstrual   disorders   complicating  ado- 
lescent goiter,   179 
disturbance  in  forme   fruste,  183 
Metabolic  disturbances  as  aid  in  goiter 

diagnosis,  116 
Metastatic  thyroid  tumors,  147 
Morphology  of  the  thyroid  gland,  28 
Mortality  after  operation,  131 
Muscular  fatigue  in  goiter,  94 

system   in   goiter,   83,   94 
Muscles,  anesthetization  of,  211 
of  the  neck,  188,  191 
incision  of,  215 
Myocardial  changes  in  colloid    goiters, 

50 
Mj'xedema  in  colloid  goiter,  55 
postoperative,  173 

N 

Neck  muscles,  188 
Nerve  compression  in  goiter,  136 
supply  of  neck,  192 

of  skin  and  muscles,  190 
of  thyroid  gland,  193 
Nerves  of  the  thyroid  gland,  34 
superior  laryngeal,  193 
sympathetic,   193 
condition  in  forme  fruste,  121 
Nervous  svstem,  pathology  of,  in  goiter, 

79 
Nervousness    and    restlessness,    postop- 
erative, in  goiter,  162 
Neurogenic  theories,  23 
Neuropathic    tachycardia    in    diagnosis 

of  toxic  goiter,  117 
Nontoxic     goiter,     preoperative     treat- 
ment, 156 
Novocaine  in  goiter  operation,  207 
Nystagmus,  93 


Operation    {see  goiter  operation) 

Operations  on  the  thyroid  gland,"  tech- 
nic  of,  205 

Operative  treatment  for  adolescent  goi- 
ter, dependent  on  patient's 
general  health,  178 

Organic  disturbances  in  relation  to  goi- 
ter,  115 

Osseous  system  in  goiter,  84 

Ovarian  hypoplasia  associated  with 
forme   fruste,  122 


Pain,  postoperative,  in  goiter,  162 
Pancreas,  pathology  of,  in  goiter,   82 
Papillary  type  of  adenomatous  goiter,  66 
Paralysis  of  vocal  cords,  postoperative, 

168 
Parathyroids,   pathology  of,   in   goiter, 

82 
Pathogenesis  of  goiter,  17 
Pathologic   anatomy,   41 
Pathology   of   goiter,    classification   of, 
41 

of  other  organs  associated  with  goi- 
ter, 79 
Pituitary  disturbances  in  goiter,  20 
Platysma,  incision  of,  214 

myoides  in  relation  to  thyroid  gland. 
186 
Pneumonia,  postoperative,  172 
Pole  ligation,  236 

stumps,  disposal  of,  229 
Polyglandular  disease,  20 
Postoperative  complications,  166 

toxemia,  163 

treatment  of  goiter,  161 
I'reoperative  treatment,  156 
Primary  toxic  goiters,  prognosis  in,  128 
Prognosis  in  disease  of  the  thyroid,  125 
I'upil  sign,  93 

R 

Rest,  part  of  preoperative  treatment  of 
toxic  goiter,  157 

Resting  colloid  goiter,  44 

Restlessness  and  nervousness,  postop- 
erative, in  goiter,  162 

S 

Saber  sheath  trachea,  133 
Scars  following  operation,  171 
Secondary  adenomatous  goiter,   74 

Basedow,  71 

degeneration,  prognosis  in,  12P 

toxic  goiter,  71 
diagnosis  of,  117 
treatment  of,  181 

toxicity,  diagnosis  of,  114 
Sensitiveness  of  goiter,  88 
Sex  in  relation  to  goiter,  18 
Shock  in  etiology  of  goiter,  24 

postoperative,  169 
Simple  colloid  goiters,  diagnosis  of,  113 
Skin  changes  in  goiter,  104 

closure   of,  235 

covering  thyroid  gland,  185 

incision,  in  goiter  operation,  214 
Sternohyoid  muscles,  restoration  of,  233 
SternomastoM  muscles,  188 
Sternothyroid  muscle,  188 


244 


INDEX 


Submaxillary    region,    aljorrant    tumors 

of,   151 
Substernal  goiter,   diflferentiation   from 
Graves'  disease,  140 
hemorrhage  into,  145 
incidence,    140 
treatment,  147 
Superficial  veins,  180 
Superior  pole,  isolation  of,  217 
Suprarenal  gland  pathology   in   goiter, 

82 
Suspensory  ligament,   artery  to,   196 
Sutures   used   in   goiter   operation,   233 
Sympathetic  nerves,  193 
Symptomatology  of  goiter,  85 
Symptoms  of  abnormally  situated  goi- 
ters, 142 


Tacliycardia  and  tremor  in  diagnosis  of 
toxic  goiter,  117 
in  goiter,  96 
Tear  secretion  in  goiter,  93 
Temperature,  control  of,  postoperative, 

162 
Tetany,  postoperative,  172 
Thymus,  pathology  of,  in  goiter,  80 

tumors,    146 
Thyroglossal  cysts,  152 
Thyrogenic  theory  in  goiter,  25 
Thyroid  arteries,  inferior,  198 

and  veins,  inferior,  ligation  of,  223 
artery,  superior,  31 
cysts  of  the,  53 
disease,  diagnosis  of,  112 
prognosis  in,  125 
symptomatology  of,   85 
diseases   {see  also  goiter),   80 
gland,    abnormal    expansion    of    nor- 
mally situated,  133 
accessory,  149 
acini,  34 
adenomas  of,  59 
anatomy  of,  28 
arteries  of,  196 
superior,  196 
blood  supply  of,  194  f 

vessels  of,  32 
capsule,  28 
consistency  of,  87 
disease,  degree  of  enlargement,  85 
false  capsule  in  relation  to,  190 
interacinal  cells  in,  37 
lymph  vessels,  34 
morphology  of,  28 
muscles  of  neck  in  relation  to,  188 
nerve  supply  of,  193 

of  skin  and  muscles,  190 
nerves  of,  34 


Thyroid  gland— Cont'd. 

platysma    myoides    in    relation   to^ 

186 
relation  of,  to  genital  function,  18 
resection  of,  226 
skin  covering,  185 
superficial  veins,  186 
symptomatology  of  disease  of,  85 
technic  of  operations  on,  205 
topographic  anatomy  of,  185 
topography  of,  194 
treatment  of  diseases  of,  175 
hypertrophy,   disturbance   of   site   of 

vessels  by,  200 
nodules  at  base  of  tongue,  150 
veins,  202 
Thyroidea  ima  artery,  198 

ima  vein,  202 
Thyrotoxic  heart,  100 
Topographic  anatomy  of  thyroid  gland, 

185 
Topography  of- lateral  veins,,  223 
Toxemia,    postoperative,    treatment    of, 

163 
Toxic  goiter,  39 

classification  of,  116 
diagnosis  of,  116 

diet  in  preoperative  treatment,  158 
drugs  in,   159 
papillary  formation  in,  67 
preliminary  examination,  156 
preoperative  treatment,  156 
primary  treatment  of,  181 
prognosis  in,   128 

rest  in  preoperative  treatment,  157 
time  of  operation,  160 
vomiting  and  diarrhea  in,  160 
Toxicity  of  goiters,  recessions  in,   70 
Trachea,  collapse  of,  postoperative,,  166 
compression  of,  by  goiter,  134,  135 
displacement  of,  by  goiter,  136 
disturbance  as  aid  in  diagnosis  of  ab- 
normally situated  goiter,  144 
Tracheitis,  postoperative,  163 
Treatment   of   diseases  of  the   thyroid, 

175 
Tremor  as  symptom  of  goiter,  94 
Tuberculosis,    differentiation    of,    from 
toxic  goiter,   117 

U 

Urticarial  lesions,  105 

V 

Vascularity  of  the  thyroid  gland,  32 
Veins,  thyroid,  202 


INDEX 


245 


Vessels,  compression  of,  by  goiter,  133 
disturbance    of    site    of,   by    thyroid 

hypertrophy,  200 
to  isthmus,  ligation  of,  219 
t,A"pical  sites  of  ligation  of,  202 

Vision,  field   of,  93 

Vocal  cords,  paralysis  of,  postoperative, 
168 

Voice,  loss  of,  postoperative,  168 

"N^omiting  in   goiter,   102 

and  diarrhea  in  toxic  goiter,  160 
postoperative,  in  goiter  cases,  161 


W 

Wandering  goiter,  140 
AVater  in  relation  to  goiter,  21 
Winking,  lessening  of  involuntaryj  91 
Worry,    influence    of,    in    toxic    goiter 

cases,  157 
Wound,  care  of,  164 
closure  of,  230 


X-ray  examination  in  goiter,  86 


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